A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal dis...
Ausführliche Beschreibung
Autor*in: |
Pey, Roxana [verfasserIn] Bach, Jürgen - 1969- [verfasserIn] Schieren, Gisela [verfasserIn] Gretz, Norbert - 1954-2023 [verfasserIn] Hafner, Mathias - 1956- [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
November-December 1999 |
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Schlagwörter: |
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Anmerkung: |
Gesehen am 09.06.2022 |
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Umfang: |
Illustrationen 9 |
Übergeordnetes Werk: |
Enthalten in: In vitro cellular & developmental biology. Animal - Berlin : Springer, 1993, 35(1999), 10 vom: Nov./Dez., Seite 571-579 |
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Übergeordnetes Werk: |
volume:35 ; year:1999 ; number:10 ; month:11/12 ; pages:571-579 ; extent:9 |
Links: |
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DOI / URN: |
10.1007/s11626-999-0095-4 |
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Katalog-ID: |
1806553112 |
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100 | 1 | |a Pey, Roxana |e verfasserin |0 (DE-588)1259479668 |0 (DE-627)1806553724 |4 aut | |
245 | 1 | 2 | |a A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease |c Roxana Pey, Juergen Bach, Gisela Schieren, Norbert Gretz, Mathias Hafner |
264 | 1 | |c [November-December 1999] | |
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520 | |a Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. | ||
650 | 4 | |a ADPKD | |
650 | 4 | |a cell culture | |
650 | 4 | |a cystogenesis | |
650 | 4 | |a EGF | |
650 | 4 | |a renal cyst | |
650 | 4 | |a taxol | |
700 | 1 | |a Bach, Jürgen |d 1969- |e verfasserin |0 (DE-588)121830616 |0 (DE-627)705669467 |0 (DE-576)292907346 |4 aut | |
700 | 1 | |a Schieren, Gisela |e verfasserin |0 (DE-588)1259480860 |0 (DE-627)1806554844 |4 aut | |
700 | 1 | |a Gretz, Norbert |d 1954-2023 |e verfasserin |0 (DE-588)1020104589 |0 (DE-627)691105154 |0 (DE-576)359544843 |4 aut | |
700 | 1 | |a Hafner, Mathias |d 1956- |e verfasserin |0 (DE-588)1027781187 |0 (DE-627)729718379 |0 (DE-576)375302956 |4 aut | |
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912 | |a GBV_ILN_293 | ||
912 | |a GBV_ILN_370 | ||
912 | |a GBV_ILN_374 | ||
912 | |a GBV_ILN_602 | ||
912 | |a GBV_ILN_636 | ||
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912 | |a GBV_ILN_702 | ||
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912 | |a GBV_ILN_2004 | ||
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912 | |a GBV_ILN_2014 | ||
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912 | |a GBV_ILN_2143 | ||
912 | |a GBV_ILN_2144 | ||
912 | |a GBV_ILN_2147 | ||
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912 | |a GBV_ILN_2158 | ||
912 | |a GBV_ILN_2188 | ||
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912 | |a GBV_ILN_2336 | ||
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1999 |
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10.1007/s11626-999-0095-4 doi (DE-627)1806553112 (DE-599)KXP1806553112 (OCoLC)1341461165 DE-627 ger DE-627 rda eng Pey, Roxana verfasserin (DE-588)1259479668 (DE-627)1806553724 aut A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease Roxana Pey, Juergen Bach, Gisela Schieren, Norbert Gretz, Mathias Hafner [November-December 1999] Illustrationen 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.06.2022 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. ADPKD cell culture cystogenesis EGF renal cyst taxol Bach, Jürgen 1969- verfasserin (DE-588)121830616 (DE-627)705669467 (DE-576)292907346 aut Schieren, Gisela verfasserin (DE-588)1259480860 (DE-627)1806554844 aut Gretz, Norbert 1954-2023 verfasserin (DE-588)1020104589 (DE-627)691105154 (DE-576)359544843 aut Hafner, Mathias 1956- verfasserin (DE-588)1027781187 (DE-627)729718379 (DE-576)375302956 aut Enthalten in In vitro cellular & developmental biology. Animal Berlin : Springer, 1993 35(1999), 10 vom: Nov./Dez., Seite 571-579 Online-Ressource (DE-627)345200888 (DE-600)2074849-8 (DE-576)102554137 1543-706X nnns volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 https://doi.org/10.1007/s11626-999-0095-4 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2808 GBV_ILN_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 35 1999 10 11/12 571-579 9 2013 01 DE-16-250 4146509289 00 --%%-- --%%-- --%%-- --%%-- l01 09-06-22 2013 01 DE-16-250 00 s hd1999 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_5 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1806554984 Bach, Jürgen 2013 01 DE-16-250 04 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1806555174 Schieren, Gisela 2013 01 DE-16-250 05 k (DE-627)141646865X V. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1429542683 Gretz, Norbert 2013 01 DE-16-250 06 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 |
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10.1007/s11626-999-0095-4 doi (DE-627)1806553112 (DE-599)KXP1806553112 (OCoLC)1341461165 DE-627 ger DE-627 rda eng Pey, Roxana verfasserin (DE-588)1259479668 (DE-627)1806553724 aut A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease Roxana Pey, Juergen Bach, Gisela Schieren, Norbert Gretz, Mathias Hafner [November-December 1999] Illustrationen 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.06.2022 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. ADPKD cell culture cystogenesis EGF renal cyst taxol Bach, Jürgen 1969- verfasserin (DE-588)121830616 (DE-627)705669467 (DE-576)292907346 aut Schieren, Gisela verfasserin (DE-588)1259480860 (DE-627)1806554844 aut Gretz, Norbert 1954-2023 verfasserin (DE-588)1020104589 (DE-627)691105154 (DE-576)359544843 aut Hafner, Mathias 1956- verfasserin (DE-588)1027781187 (DE-627)729718379 (DE-576)375302956 aut Enthalten in In vitro cellular & developmental biology. Animal Berlin : Springer, 1993 35(1999), 10 vom: Nov./Dez., Seite 571-579 Online-Ressource (DE-627)345200888 (DE-600)2074849-8 (DE-576)102554137 1543-706X nnns volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 https://doi.org/10.1007/s11626-999-0095-4 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2808 GBV_ILN_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 35 1999 10 11/12 571-579 9 2013 01 DE-16-250 4146509289 00 --%%-- --%%-- --%%-- --%%-- l01 09-06-22 2013 01 DE-16-250 00 s hd1999 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_5 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1806554984 Bach, Jürgen 2013 01 DE-16-250 04 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1806555174 Schieren, Gisela 2013 01 DE-16-250 05 k (DE-627)141646865X V. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1429542683 Gretz, Norbert 2013 01 DE-16-250 06 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 |
allfields_unstemmed |
10.1007/s11626-999-0095-4 doi (DE-627)1806553112 (DE-599)KXP1806553112 (OCoLC)1341461165 DE-627 ger DE-627 rda eng Pey, Roxana verfasserin (DE-588)1259479668 (DE-627)1806553724 aut A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease Roxana Pey, Juergen Bach, Gisela Schieren, Norbert Gretz, Mathias Hafner [November-December 1999] Illustrationen 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.06.2022 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. ADPKD cell culture cystogenesis EGF renal cyst taxol Bach, Jürgen 1969- verfasserin (DE-588)121830616 (DE-627)705669467 (DE-576)292907346 aut Schieren, Gisela verfasserin (DE-588)1259480860 (DE-627)1806554844 aut Gretz, Norbert 1954-2023 verfasserin (DE-588)1020104589 (DE-627)691105154 (DE-576)359544843 aut Hafner, Mathias 1956- verfasserin (DE-588)1027781187 (DE-627)729718379 (DE-576)375302956 aut Enthalten in In vitro cellular & developmental biology. Animal Berlin : Springer, 1993 35(1999), 10 vom: Nov./Dez., Seite 571-579 Online-Ressource (DE-627)345200888 (DE-600)2074849-8 (DE-576)102554137 1543-706X nnns volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 https://doi.org/10.1007/s11626-999-0095-4 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2808 GBV_ILN_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 35 1999 10 11/12 571-579 9 2013 01 DE-16-250 4146509289 00 --%%-- --%%-- --%%-- --%%-- l01 09-06-22 2013 01 DE-16-250 00 s hd1999 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_5 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1806554984 Bach, Jürgen 2013 01 DE-16-250 04 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1806555174 Schieren, Gisela 2013 01 DE-16-250 05 k (DE-627)141646865X V. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1429542683 Gretz, Norbert 2013 01 DE-16-250 06 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 |
allfieldsGer |
10.1007/s11626-999-0095-4 doi (DE-627)1806553112 (DE-599)KXP1806553112 (OCoLC)1341461165 DE-627 ger DE-627 rda eng Pey, Roxana verfasserin (DE-588)1259479668 (DE-627)1806553724 aut A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease Roxana Pey, Juergen Bach, Gisela Schieren, Norbert Gretz, Mathias Hafner [November-December 1999] Illustrationen 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.06.2022 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. ADPKD cell culture cystogenesis EGF renal cyst taxol Bach, Jürgen 1969- verfasserin (DE-588)121830616 (DE-627)705669467 (DE-576)292907346 aut Schieren, Gisela verfasserin (DE-588)1259480860 (DE-627)1806554844 aut Gretz, Norbert 1954-2023 verfasserin (DE-588)1020104589 (DE-627)691105154 (DE-576)359544843 aut Hafner, Mathias 1956- verfasserin (DE-588)1027781187 (DE-627)729718379 (DE-576)375302956 aut Enthalten in In vitro cellular & developmental biology. Animal Berlin : Springer, 1993 35(1999), 10 vom: Nov./Dez., Seite 571-579 Online-Ressource (DE-627)345200888 (DE-600)2074849-8 (DE-576)102554137 1543-706X nnns volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 https://doi.org/10.1007/s11626-999-0095-4 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2808 GBV_ILN_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 35 1999 10 11/12 571-579 9 2013 01 DE-16-250 4146509289 00 --%%-- --%%-- --%%-- --%%-- l01 09-06-22 2013 01 DE-16-250 00 s hd1999 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_5 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1806554984 Bach, Jürgen 2013 01 DE-16-250 04 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1806555174 Schieren, Gisela 2013 01 DE-16-250 05 k (DE-627)141646865X V. Medizinische Klinik 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_3 2013 01 DE-16-250 06 p (DE-627)1429542683 Gretz, Norbert 2013 01 DE-16-250 06 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 |
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10.1007/s11626-999-0095-4 doi (DE-627)1806553112 (DE-599)KXP1806553112 (OCoLC)1341461165 DE-627 ger DE-627 rda eng Pey, Roxana verfasserin (DE-588)1259479668 (DE-627)1806553724 aut A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease Roxana Pey, Juergen Bach, Gisela Schieren, Norbert Gretz, Mathias Hafner [November-December 1999] Illustrationen 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.06.2022 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. ADPKD cell culture cystogenesis EGF renal cyst taxol Bach, Jürgen 1969- verfasserin (DE-588)121830616 (DE-627)705669467 (DE-576)292907346 aut Schieren, Gisela verfasserin (DE-588)1259480860 (DE-627)1806554844 aut Gretz, Norbert 1954-2023 verfasserin (DE-588)1020104589 (DE-627)691105154 (DE-576)359544843 aut Hafner, Mathias 1956- verfasserin (DE-588)1027781187 (DE-627)729718379 (DE-576)375302956 aut Enthalten in In vitro cellular & developmental biology. Animal Berlin : Springer, 1993 35(1999), 10 vom: Nov./Dez., Seite 571-579 Online-Ressource (DE-627)345200888 (DE-600)2074849-8 (DE-576)102554137 1543-706X nnns volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 https://doi.org/10.1007/s11626-999-0095-4 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_121 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2043 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2158 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2193 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_2808 GBV_ILN_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 35 1999 10 11/12 571-579 9 2013 01 DE-16-250 4146509289 00 --%%-- --%%-- --%%-- --%%-- l01 09-06-22 2013 01 DE-16-250 00 s hd1999 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_5 2013 01 DE-16-250 03 s s_9 2013 01 DE-16-250 04 p (DE-627)1806554984 Bach, Jürgen 2013 01 DE-16-250 04 k (DE-627)1426595557 Zentrum für Medizinische Forschung 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_2 2013 01 DE-16-250 05 p (DE-627)1806555174 Schieren, Gisela 2013 01 DE-16-250 05 k (DE-627)141646865X V. 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Enthalten in In vitro cellular & developmental biology. Animal 35(1999), 10 vom: Nov./Dez., Seite 571-579 volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 |
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Enthalten in In vitro cellular & developmental biology. Animal 35(1999), 10 vom: Nov./Dez., Seite 571-579 volume:35 year:1999 number:10 month:11/12 pages:571-579 extent:9 |
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ADPKD cell culture cystogenesis EGF renal cyst taxol |
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In vitro cellular & developmental biology. Animal |
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Pey, Roxana @@aut@@ Bach, Jürgen @@aut@@ Schieren, Gisela @@aut@@ Gretz, Norbert @@aut@@ Hafner, Mathias @@aut@@ |
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Elektronische Aufsätze |
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new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease |
title_auth |
A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease |
abstract |
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. Gesehen am 09.06.2022 |
abstractGer |
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. Gesehen am 09.06.2022 |
abstract_unstemmed |
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequent human inherited diseases. The main feature of the disease is the development of renal cysts, first occurring in the proximal tubules, and with time, dominating all segments of the nephron, leading to end-stage renal disease in 50% of the patients in their fifth decade of life. A therapy for polycystic kidney disease (PKD) has not yet been developed. Patients coming to end-stage ADPKD require long-term dialysis and/or transplantation. A suitable animal model to study ADPKD is the spontaneously mutated Han:SPRD (cy/ +) rat, but a method to cultivate Han:SPRD (cy/ +) derived renal cells which preserves their ability to form cyst-like structures in vitro has previously not been reported. Based on this well-characterized animal model, we developed a cell culture model of renal cyst formation in vitro. When renal cells of the Han:SPRD (cy/ +) rat were isolated and cultured under conditions that prevent cell-substratum adhesion, large amounts of cyst-like structures were formed de novo from Han:SPRD (cy/ +) derived renal cells, but only a few from control rat renal cells. In contrast, when cultivated on plastic as monolayer cultures, Han:SPRD (cy/ +)-derived and control rat-derived renal cells were indistinguishable and did not form cyst-like structures. Immunohistochemical characterization of the cyst-like structures suggests tubular epithelial origin of the cyst-forming cells. The amount of cysts formed from Han:SPRD (cy/ +)-derived renal cells grown in a stationary suspension culture is susceptible to modulation by different conditions. Human cyst fluid and epidermal growth factor both stimulated the formation of cysts from Han:SPRD (cy/ +)-derived renal cells whereas taxol inhibited cystogenesis. In contrast, neither human cyst fluid nor epidermal growth factor affected the amount of cysts formed by control rat renal cells. As the culture model reported here allows not only the distinction of PKD-derived tubular epithelium from its normal counterpart, but also the modulation of cyst formation especially by Han:SPRD (cy/ +)-derived renal cells, it might be a useful prescreening protocol for potential treatments for PKD and thus reduce the need for animal experiments. Gesehen am 09.06.2022 |
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A new in vitro bioassay for cyst formation by renal cells from an autosomal dominant rat model of polycystic kidney disease |
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