Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor
Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I a...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Okazaki, Yuko [verfasserIn] Yamasaki, Yasushi [verfasserIn] Uchida, Haruhito A. [verfasserIn] Okamoto, Kazunori [verfasserIn] Satoh, Minoru [verfasserIn] Maruyama, Keisuke [verfasserIn] Maeshima, Yohei [verfasserIn] Sugiyama, Hitoshi [verfasserIn] Sugaya, Takeshi [verfasserIn] Kashihara, Naoki [verfasserIn] Makino, Hirofumi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Übergeordnetes Werk: |
Enthalten in: Clinical and experimental nephrology - [Tokyo] : Springer, 1997, 11(2007), 1 vom: März, Seite 77-87 |
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| Übergeordnetes Werk: |
volume:11 ; year:2007 ; number:1 ; month:03 ; pages:77-87 |
| Links: |
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| DOI / URN: |
10.1007/s10157-006-0456-1 |
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| Katalog-ID: |
SPR008961670 |
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| 100 | 1 | |a Okazaki, Yuko |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor |
| 264 | 1 | |c 2007 | |
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| 520 | |a Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. | ||
| 700 | 1 | |a Yamasaki, Yasushi |e verfasserin |4 aut | |
| 700 | 1 | |a Uchida, Haruhito A. |e verfasserin |4 aut | |
| 700 | 1 | |a Okamoto, Kazunori |e verfasserin |4 aut | |
| 700 | 1 | |a Satoh, Minoru |e verfasserin |4 aut | |
| 700 | 1 | |a Maruyama, Keisuke |e verfasserin |4 aut | |
| 700 | 1 | |a Maeshima, Yohei |e verfasserin |4 aut | |
| 700 | 1 | |a Sugiyama, Hitoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Sugaya, Takeshi |e verfasserin |4 aut | |
| 700 | 1 | |a Kashihara, Naoki |e verfasserin |4 aut | |
| 700 | 1 | |a Makino, Hirofumi |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Clinical and experimental nephrology |d [Tokyo] : Springer, 1997 |g 11(2007), 1 vom: März, Seite 77-87 |w (DE-627)306646900 |w (DE-600)1499111-1 |x 1437-7799 |7 nnns |
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2007 |
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10.1007/s10157-006-0456-1 doi (DE-627)SPR008961670 (SPR)s10157-006-0456-1-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Okazaki, Yuko verfasserin aut Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. Yamasaki, Yasushi verfasserin aut Uchida, Haruhito A. verfasserin aut Okamoto, Kazunori verfasserin aut Satoh, Minoru verfasserin aut Maruyama, Keisuke verfasserin aut Maeshima, Yohei verfasserin aut Sugiyama, Hitoshi verfasserin aut Sugaya, Takeshi verfasserin aut Kashihara, Naoki verfasserin aut Makino, Hirofumi verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 1 vom: März, Seite 77-87 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:1 month:03 pages:77-87 https://dx.doi.org/10.1007/s10157-006-0456-1 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 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_602 GBV_ILN_636 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_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_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 1 03 77-87 |
| spelling |
10.1007/s10157-006-0456-1 doi (DE-627)SPR008961670 (SPR)s10157-006-0456-1-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Okazaki, Yuko verfasserin aut Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. Yamasaki, Yasushi verfasserin aut Uchida, Haruhito A. verfasserin aut Okamoto, Kazunori verfasserin aut Satoh, Minoru verfasserin aut Maruyama, Keisuke verfasserin aut Maeshima, Yohei verfasserin aut Sugiyama, Hitoshi verfasserin aut Sugaya, Takeshi verfasserin aut Kashihara, Naoki verfasserin aut Makino, Hirofumi verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 1 vom: März, Seite 77-87 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:1 month:03 pages:77-87 https://dx.doi.org/10.1007/s10157-006-0456-1 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 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_602 GBV_ILN_636 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_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_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 1 03 77-87 |
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10.1007/s10157-006-0456-1 doi (DE-627)SPR008961670 (SPR)s10157-006-0456-1-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Okazaki, Yuko verfasserin aut Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. Yamasaki, Yasushi verfasserin aut Uchida, Haruhito A. verfasserin aut Okamoto, Kazunori verfasserin aut Satoh, Minoru verfasserin aut Maruyama, Keisuke verfasserin aut Maeshima, Yohei verfasserin aut Sugiyama, Hitoshi verfasserin aut Sugaya, Takeshi verfasserin aut Kashihara, Naoki verfasserin aut Makino, Hirofumi verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 1 vom: März, Seite 77-87 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:1 month:03 pages:77-87 https://dx.doi.org/10.1007/s10157-006-0456-1 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 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_602 GBV_ILN_636 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_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_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 1 03 77-87 |
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10.1007/s10157-006-0456-1 doi (DE-627)SPR008961670 (SPR)s10157-006-0456-1-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Okazaki, Yuko verfasserin aut Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. Yamasaki, Yasushi verfasserin aut Uchida, Haruhito A. verfasserin aut Okamoto, Kazunori verfasserin aut Satoh, Minoru verfasserin aut Maruyama, Keisuke verfasserin aut Maeshima, Yohei verfasserin aut Sugiyama, Hitoshi verfasserin aut Sugaya, Takeshi verfasserin aut Kashihara, Naoki verfasserin aut Makino, Hirofumi verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 1 vom: März, Seite 77-87 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:1 month:03 pages:77-87 https://dx.doi.org/10.1007/s10157-006-0456-1 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 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_602 GBV_ILN_636 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_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_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 1 03 77-87 |
| allfieldsSound |
10.1007/s10157-006-0456-1 doi (DE-627)SPR008961670 (SPR)s10157-006-0456-1-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Okazaki, Yuko verfasserin aut Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. Yamasaki, Yasushi verfasserin aut Uchida, Haruhito A. verfasserin aut Okamoto, Kazunori verfasserin aut Satoh, Minoru verfasserin aut Maruyama, Keisuke verfasserin aut Maeshima, Yohei verfasserin aut Sugiyama, Hitoshi verfasserin aut Sugaya, Takeshi verfasserin aut Kashihara, Naoki verfasserin aut Makino, Hirofumi verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 1 vom: März, Seite 77-87 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:1 month:03 pages:77-87 https://dx.doi.org/10.1007/s10157-006-0456-1 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_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_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 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_602 GBV_ILN_636 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_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_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 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_2188 GBV_ILN_2190 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_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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 1 03 77-87 |
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Enthalten in Clinical and experimental nephrology 11(2007), 1 vom: März, Seite 77-87 volume:11 year:2007 number:1 month:03 pages:77-87 |
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Enthalten in Clinical and experimental nephrology 11(2007), 1 vom: März, Seite 77-87 volume:11 year:2007 number:1 month:03 pages:77-87 |
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Clinical and experimental nephrology |
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Okazaki, Yuko @@aut@@ Yamasaki, Yasushi @@aut@@ Uchida, Haruhito A. @@aut@@ Okamoto, Kazunori @@aut@@ Satoh, Minoru @@aut@@ Maruyama, Keisuke @@aut@@ Maeshima, Yohei @@aut@@ Sugiyama, Hitoshi @@aut@@ Sugaya, Takeshi @@aut@@ Kashihara, Naoki @@aut@@ Makino, Hirofumi @@aut@@ |
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2007-03-01T00:00:00Z |
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AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yamasaki, Yasushi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Uchida, Haruhito A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Okamoto, Kazunori</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Satoh, Minoru</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Maruyama, 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Okazaki, Yuko |
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Okazaki, Yuko ddc 610 bkl 44.88 Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor |
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610 ASE 44.88 bkl Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor |
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Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor |
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Okazaki, Yuko |
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Clinical and experimental nephrology |
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Okazaki, Yuko Yamasaki, Yasushi Uchida, Haruhito A. Okamoto, Kazunori Satoh, Minoru Maruyama, Keisuke Maeshima, Yohei Sugiyama, Hitoshi Sugaya, Takeshi Kashihara, Naoki Makino, Hirofumi |
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Elektronische Aufsätze |
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Okazaki, Yuko |
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enhanced tgf-b/smad signaling in the early stage of diabetic nephropathy is independent of the at1a receptor |
| title_auth |
Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor |
| abstract |
Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. |
| abstractGer |
Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. |
| abstract_unstemmed |
Background Angiotensin II (AII) and transforming growth factor-β (TGF-β) are closely involved in the pathogenesis of diabetic nephropathy (DN). AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. Results The expression of both TGF-βRI and RII was up-regulated in the glomerular tufts and vasculature in diabetic $ AT1a^{+/+} $ mice kidney by immunohistochemistry. RT–PCR revealed that mRNAs for TGF-βRI and RII were also up-regulated. Smad2 and 4 protein levels were reduced in the renal cortex after the induction of diabetes, with an increase of Smad 3/4 complex in the nucleus. The expression of TGF-β receptors increased in both diabetic $ AT1a^{−/−} $ and $ AT1a^{+/+} $ mice. Smad signaling in $ AT1a^{−/−} $ mice was also enhanced. Conclusions Our results suggest that the complete blockade of the AT1a-mediated pathway has a minimal effect on the enhanced TGF-β/Smad signaling in the early stage of DN, at least in the $ AT1a^{−/−} $ model. |
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Enhanced TGF-b/Smad signaling in the early stage of diabetic nephropathy is independent of the AT1a receptor |
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Yamasaki, Yasushi Uchida, Haruhito A. Okamoto, Kazunori Satoh, Minoru Maruyama, Keisuke Maeshima, Yohei Sugiyama, Hitoshi Sugaya, Takeshi Kashihara, Naoki Makino, Hirofumi |
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Yamasaki, Yasushi Uchida, Haruhito A. Okamoto, Kazunori Satoh, Minoru Maruyama, Keisuke Maeshima, Yohei Sugiyama, Hitoshi Sugaya, Takeshi Kashihara, Naoki Makino, Hirofumi |
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AII is known to induce TGF-β production in resident renal cells, including glomerular mesangial cells and tubular epithelial cells. TGF-β receptor types I and II (TGF-βRI, II) are up-regulated in the diabetic kidney. The aim of this study was to clarify the role of AII in the regulation of the TGF-β system in the early stage of DN using AII type1a receptor-deficient($ AT1a^{−/−} $) mice. Methods We investigated the expression of TGF-β1, TGF-βRI, II, and Smad signaling in $ AT1a^{−/−} $ mice with streptozotocin (STZ)-induced DN. Mice were killed 10 and 20 days after the induction of hyperglycemia. The expression of TGF-β receptors was analyzed by immunohistochemical staining and reverse transcriptase–polymerase chain reaction (RT–PCR). TGF-β-specific Smad signaling was analyzed by electrophoretic mobility shift assay and Western blotting. 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| score |
7.399453 |