Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species

Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II int...
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Gespeichert in:

Autor*in:	Wolf, Gunter [verfasserIn] Wenzel, Ulrich Hannken, Tete Stahl, Rolf A.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2001

Anmerkung:	© Springer-Verlag 2001

Übergeordnetes Werk:	Enthalten in: Journal of molecular medicine - Berlin : Springer, 1922, 79(2001), 7 vom: 19. Juni, Seite 382-389
Übergeordnetes Werk:	volume:79 ; year:2001 ; number:7 ; day:19 ; month:06 ; pages:382-389

Links:	Volltext

DOI / URN:	10.1007/s001090100241

Katalog-ID:	SPR00075028X

Internformat


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100	1		\|a Wolf, Gunter \|e verfasserin \|4 aut
245	1	0	\|a Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
264		1	\|c 2001
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520			\|a Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells.
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700	1		\|a Hannken, Tete \|4 aut
700	1		\|a Stahl, Rolf A. \|4 aut
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856	4	0	\|u https://dx.doi.org/10.1007/s001090100241 \|z lizenzpflichtig \|3 Volltext
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912			\|a GBV_ILN_187
912			\|a GBV_ILN_206
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912			\|a GBV_ILN_230
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912			\|a GBV_ILN_281
912			\|a GBV_ILN_285
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
912			\|a GBV_ILN_647
912			\|a GBV_ILN_702
912			\|a GBV_ILN_711
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2004
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2007
912			\|a GBV_ILN_2008
912			\|a GBV_ILN_2009
912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2015
912			\|a GBV_ILN_2018
912			\|a GBV_ILN_2020
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912			\|a GBV_ILN_2026
912			\|a GBV_ILN_2027
912			\|a GBV_ILN_2031
912			\|a GBV_ILN_2034
912			\|a GBV_ILN_2037
912			\|a GBV_ILN_2038
912			\|a GBV_ILN_2039
912			\|a GBV_ILN_2043
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
912			\|a GBV_ILN_2049
912			\|a GBV_ILN_2050
912			\|a GBV_ILN_2055
912			\|a GBV_ILN_2056
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2059
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2093
912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2107
912			\|a GBV_ILN_2108
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912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2112
912			\|a GBV_ILN_2113
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912			\|a GBV_ILN_2118
912			\|a GBV_ILN_2119
912			\|a GBV_ILN_2122
912			\|a GBV_ILN_2129
912			\|a GBV_ILN_2143
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912			\|a GBV_ILN_4037
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912			\|a GBV_ILN_4125
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912			\|a GBV_ILN_4335
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912			\|a GBV_ILN_4346
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952			\|d 79 \|j 2001 \|e 7 \|b 19 \|c 06 \|h 382-389

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author_variant	g w gw u w uw t h th r a s ra ras
matchkey_str	article:14321440:2001----::nitniiidcs2kpepesoirnluueivvrlo
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publishDate	2001
allfields	10.1007/s001090100241 doi (DE-627)SPR00075028X (SPR)s001090100241-e DE-627 ger DE-627 rakwb eng Wolf, Gunter verfasserin aut Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2001 Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. Wenzel, Ulrich aut Hannken, Tete aut Stahl, Rolf A. aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 79(2001), 7 vom: 19. Juni, Seite 382-389 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:79 year:2001 number:7 day:19 month:06 pages:382-389 https://dx.doi.org/10.1007/s001090100241 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 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_711 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_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 79 2001 7 19 06 382-389
spelling	10.1007/s001090100241 doi (DE-627)SPR00075028X (SPR)s001090100241-e DE-627 ger DE-627 rakwb eng Wolf, Gunter verfasserin aut Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2001 Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. Wenzel, Ulrich aut Hannken, Tete aut Stahl, Rolf A. aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 79(2001), 7 vom: 19. Juni, Seite 382-389 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:79 year:2001 number:7 day:19 month:06 pages:382-389 https://dx.doi.org/10.1007/s001090100241 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 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_711 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_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 79 2001 7 19 06 382-389
allfields_unstemmed	10.1007/s001090100241 doi (DE-627)SPR00075028X (SPR)s001090100241-e DE-627 ger DE-627 rakwb eng Wolf, Gunter verfasserin aut Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2001 Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. Wenzel, Ulrich aut Hannken, Tete aut Stahl, Rolf A. aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 79(2001), 7 vom: 19. Juni, Seite 382-389 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:79 year:2001 number:7 day:19 month:06 pages:382-389 https://dx.doi.org/10.1007/s001090100241 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 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_711 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_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 79 2001 7 19 06 382-389
allfieldsGer	10.1007/s001090100241 doi (DE-627)SPR00075028X (SPR)s001090100241-e DE-627 ger DE-627 rakwb eng Wolf, Gunter verfasserin aut Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2001 Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. Wenzel, Ulrich aut Hannken, Tete aut Stahl, Rolf A. aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 79(2001), 7 vom: 19. Juni, Seite 382-389 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:79 year:2001 number:7 day:19 month:06 pages:382-389 https://dx.doi.org/10.1007/s001090100241 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 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_711 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_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 79 2001 7 19 06 382-389
allfieldsSound	10.1007/s001090100241 doi (DE-627)SPR00075028X (SPR)s001090100241-e DE-627 ger DE-627 rakwb eng Wolf, Gunter verfasserin aut Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2001 Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. Wenzel, Ulrich aut Hannken, Tete aut Stahl, Rolf A. aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 79(2001), 7 vom: 19. Juni, Seite 382-389 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:79 year:2001 number:7 day:19 month:06 pages:382-389 https://dx.doi.org/10.1007/s001090100241 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 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_711 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_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 79 2001 7 19 06 382-389
language	English
source	Enthalten in Journal of molecular medicine 79(2001), 7 vom: 19. Juni, Seite 382-389 volume:79 year:2001 number:7 day:19 month:06 pages:382-389
sourceStr	Enthalten in Journal of molecular medicine 79(2001), 7 vom: 19. Juni, Seite 382-389 volume:79 year:2001 number:7 day:19 month:06 pages:382-389
format_phy_str_mv	Article
institution	findex.gbv.de
isfreeaccess_bool	false
container_title	Journal of molecular medicine
authorswithroles_txt_mv	Wolf, Gunter @@aut@@ Wenzel, Ulrich @@aut@@ Hannken, Tete @@aut@@ Stahl, Rolf A. @@aut@@
publishDateDaySort_date	2001-06-19T00:00:00Z
hierarchy_top_id	254630804
id	SPR00075028X
language_de	englisch
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author	Wolf, Gunter
spellingShingle	Wolf, Gunter Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
authorStr	Wolf, Gunter
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topic_title	Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
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title	Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
ctrlnum	(DE-627)SPR00075028X (SPR)s001090100241-e
title_full	Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
author_sort	Wolf, Gunter
journal	Journal of molecular medicine
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author_browse	Wolf, Gunter Wenzel, Ulrich Hannken, Tete Stahl, Rolf A.
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author-letter	Wolf, Gunter
doi_str_mv	10.1007/s001090100241
title_sort	angiotensin ii induces $ p27^{kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
title_auth	Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
abstract	Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. © Springer-Verlag 2001
abstractGer	Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. © Springer-Verlag 2001
abstract_unstemmed	Abstract Previous studies have demonstrated that angiotensin II (ANG II) mediates cell cycle arrest of cultured renal tubular cells by induction of $ p27^{Kip1} $, an inhibitor of cyclin-dependent kinases. However, it is not known whether ANG II exerts similar effects in vivo. Infusion of ANG II into naive rats for 7 days increased formation of reactive oxygen species in tubular cells of the kidney. Furthermore, ANG II infusion stimulated protein expression of $ p27^{Kip1} $ as detected by western blotting of tubular lysates and immunohistochemistry. Infusion of ANG II reduced tubular proliferation as detected by proliferating-cell nuclear antigen (PCNA) immunohistochemistry. The increase in $ p27^{Kip1} $ expression was not due to an increase in mRNA. Immunoprecipitation experiments revealed that the increased $ p27^{Kip1} $ protein associates with cyclin-dependent kinase 2. Coadministration of the radical scavenger dimethylthiourea abolished this ANG II mediated $ p27^{Kip1} $ expression without reducing systemic blood pressure. Furthermore, dimethylthiourea infusion attenuates the ANG II mediated $ G_{1} $-phase arrest of tubular cells. However, infusion of norepinephrine did not induce reactive oxygen species or $ p27^{Kip1} $ expression, despite a significant increase in blood pressure. Thus ANG II induces $ p27^{Kip1} $ expression in renal tubular cells in vivo. This effect is mediated by reactive oxygen species. Since tubular hypertrophy depends on $ G_{1} $-phase arrest and may promote subsequent development of interstitial fibrosis, administering oxygen radical scavenger may be a therapeutic tool to counteract ANG II dependent remodeling of renal tubular cells. © Springer-Verlag 2001
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container_issue	7
title_short	Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species
url	https://dx.doi.org/10.1007/s001090100241
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author2	Wenzel, Ulrich Hannken, Tete Stahl, Rolf A.
author2Str	Wenzel, Ulrich Hannken, Tete Stahl, Rolf A.
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doi_str	10.1007/s001090100241
up_date	2024-07-03T18:01:05.322Z
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Angiotensin II induces $ p27^{Kip1} $ expression in renal tubules in vivo: role of reactive oxygen species

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