Direct Aldosterone Action as a Profibrotic Factor via ROS-Mediated SGK1 in Peritoneal Fibroblasts
Background/Aims: Peritoneal fibrosis leads to discontinuation of peritoneal dialysis. Although aldosterone promotes tissue fibrosis in many organs, its contribution to peritoneal fibrosis and the underlying mechanism are poorly understood. The present study investigated the direct effect of aldoster...
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| Veröffentlicht in: | Kidney & blood pressure research 2009-01, Vol.32 (3), p.185-193 |
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| creator | Yamahara, Hideki Kishimoto, Noriko Nakata, Midori Okazaki, Akiko Kimura, Taikou Sonomura, Kazuhiro Matsuoka, Eiko Shiotsu, Yayoi Adachi, Takaomi Matsubara, Hiroaki Iwasaka, Toshiji Mori, Yasukiyo |
| description | Background/Aims: Peritoneal fibrosis leads to discontinuation of peritoneal dialysis. Although aldosterone promotes tissue fibrosis in many organs, its contribution to peritoneal fibrosis and the underlying mechanism are poorly understood. The present study investigated the direct effect of aldosterone on cultured rat peritoneal fibroblasts (RPFs). Methods: The expression of aldosterone synthase (CYP11B2), mineralocorticoid receptors (MRs), 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2), serum- and glucocorticoid-inducible protein kinase 1 (SGK1), and connective tissue growth factor (CTGF) mRNA was evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). To determine the role of reactive oxygen species (ROS) induced by aldosterone, an active oxygen assay with several inhibitors was used. The ability of RPFs to produce aldosterone was examined by enzyme immunoassay. Small interfering RNA (siRNA) of SGK1 was transfected into cultured cells using lipofectamine. Results: CYP11B2, MRs, and 11β-HSD2 were expressed in RPFs. The release of aldosterone from RPFs into the culture medium was confirmed. Aldosterone increased the expression of SGK1 mRNA via ROS generation. Spironolactone, apocynin, and tempol significantly reduced SGK1 expression. Aldosterone upregulated CTGF transcripts significantly. SGK1 gene silencing suppressed aldosterone-induced CTGF expression. Conclusion: The local aldosterone system acts directly as a profibrotic factor via ROS-mediated SGK1 in RPFs. |
| doi_str_mv | 10.1159/000225379 |
| format | Article |
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Although aldosterone promotes tissue fibrosis in many organs, its contribution to peritoneal fibrosis and the underlying mechanism are poorly understood. The present study investigated the direct effect of aldosterone on cultured rat peritoneal fibroblasts (RPFs). Methods: The expression of aldosterone synthase (CYP11B2), mineralocorticoid receptors (MRs), 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2), serum- and glucocorticoid-inducible protein kinase 1 (SGK1), and connective tissue growth factor (CTGF) mRNA was evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). To determine the role of reactive oxygen species (ROS) induced by aldosterone, an active oxygen assay with several inhibitors was used. The ability of RPFs to produce aldosterone was examined by enzyme immunoassay. Small interfering RNA (siRNA) of SGK1 was transfected into cultured cells using lipofectamine. Results: CYP11B2, MRs, and 11β-HSD2 were expressed in RPFs. The release of aldosterone from RPFs into the culture medium was confirmed. Aldosterone increased the expression of SGK1 mRNA via ROS generation. Spironolactone, apocynin, and tempol significantly reduced SGK1 expression. Aldosterone upregulated CTGF transcripts significantly. SGK1 gene silencing suppressed aldosterone-induced CTGF expression. Conclusion: The local aldosterone system acts directly as a profibrotic factor via ROS-mediated SGK1 in RPFs.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000225379</identifier><identifier>PMID: 19521108</identifier><identifier>CODEN: RPBIEL</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Aldosterone - physiology ; Animals ; Cells, Cultured ; Connective Tissue Growth Factor - biosynthesis ; Gene Expression Regulation ; Immediate-Early Proteins - genetics ; Original Paper ; Peritoneal Fibrosis - etiology ; Protein-Serine-Threonine Kinases - genetics ; Rats ; Reactive Oxygen Species - metabolism ; RNA, Messenger - analysis ; RNA, Small Interfering - pharmacology</subject><ispartof>Kidney & blood pressure research, 2009-01, Vol.32 (3), p.185-193</ispartof><rights>2009 S. Karger AG, Basel</rights><rights>Copyright (c) 2009 S. Karger AG, Basel.</rights><rights>Copyright (c) 2009 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-78d3a663a464cfb545632181994d6e4749d02a9e36f98b978f39abeb35ffe10b3</citedby><cites>FETCH-LOGICAL-c332t-78d3a663a464cfb545632181994d6e4749d02a9e36f98b978f39abeb35ffe10b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19521108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamahara, Hideki</creatorcontrib><creatorcontrib>Kishimoto, Noriko</creatorcontrib><creatorcontrib>Nakata, Midori</creatorcontrib><creatorcontrib>Okazaki, Akiko</creatorcontrib><creatorcontrib>Kimura, Taikou</creatorcontrib><creatorcontrib>Sonomura, Kazuhiro</creatorcontrib><creatorcontrib>Matsuoka, Eiko</creatorcontrib><creatorcontrib>Shiotsu, Yayoi</creatorcontrib><creatorcontrib>Adachi, Takaomi</creatorcontrib><creatorcontrib>Matsubara, Hiroaki</creatorcontrib><creatorcontrib>Iwasaka, Toshiji</creatorcontrib><creatorcontrib>Mori, Yasukiyo</creatorcontrib><title>Direct Aldosterone Action as a Profibrotic Factor via ROS-Mediated SGK1 in Peritoneal Fibroblasts</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Background/Aims: Peritoneal fibrosis leads to discontinuation of peritoneal dialysis. Although aldosterone promotes tissue fibrosis in many organs, its contribution to peritoneal fibrosis and the underlying mechanism are poorly understood. The present study investigated the direct effect of aldosterone on cultured rat peritoneal fibroblasts (RPFs). Methods: The expression of aldosterone synthase (CYP11B2), mineralocorticoid receptors (MRs), 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2), serum- and glucocorticoid-inducible protein kinase 1 (SGK1), and connective tissue growth factor (CTGF) mRNA was evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). To determine the role of reactive oxygen species (ROS) induced by aldosterone, an active oxygen assay with several inhibitors was used. The ability of RPFs to produce aldosterone was examined by enzyme immunoassay. Small interfering RNA (siRNA) of SGK1 was transfected into cultured cells using lipofectamine. Results: CYP11B2, MRs, and 11β-HSD2 were expressed in RPFs. The release of aldosterone from RPFs into the culture medium was confirmed. Aldosterone increased the expression of SGK1 mRNA via ROS generation. Spironolactone, apocynin, and tempol significantly reduced SGK1 expression. Aldosterone upregulated CTGF transcripts significantly. SGK1 gene silencing suppressed aldosterone-induced CTGF expression. Conclusion: The local aldosterone system acts directly as a profibrotic factor via ROS-mediated SGK1 in RPFs.</description><subject>Aldosterone - physiology</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Connective Tissue Growth Factor - biosynthesis</subject><subject>Gene Expression Regulation</subject><subject>Immediate-Early Proteins - genetics</subject><subject>Original Paper</subject><subject>Peritoneal Fibrosis - etiology</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA, Messenger - analysis</subject><subject>RNA, Small Interfering - pharmacology</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0E1LAzEQBuAgitXqwbtI8CIeVvO1HzmWaqtYabF6XrK7s5K63dQkK_jvTW2p4Gnm8MzL8CJ0RskNpbG8JYQwFvNU7qEjKhiPCBV8_3cnkSAy6aFj5xaBxUEeoh6VMaOUZEdI3WkLpceDpjLOgzUt4EHptWmxcljhmTW1LqzxusQjVXpj8ZdW-GU6j56h0spDhefjJ4p1i2dgtQ8BqsGj9U3RKOfdCTqoVePgdDv76G10_zp8iCbT8eNwMIlKzpmP0qziKkm4Eoko6yIWccIZzaiUokpApEJWhCkJPKllVsg0q7lUBRQ8rmugpOB9dLXJXVnz2YHz-VK7EppGtWA6l6ecyyQNdQV5-U8uTGfb8FzOmKA0Cy0FdL1BpTXOWajzldVLZb9zSvJ16_mu9WAvtoFdsYTqT25rDuB8Az6UfQe7A9v7H4_2gyg</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Yamahara, Hideki</creator><creator>Kishimoto, Noriko</creator><creator>Nakata, Midori</creator><creator>Okazaki, Akiko</creator><creator>Kimura, Taikou</creator><creator>Sonomura, Kazuhiro</creator><creator>Matsuoka, Eiko</creator><creator>Shiotsu, Yayoi</creator><creator>Adachi, Takaomi</creator><creator>Matsubara, Hiroaki</creator><creator>Iwasaka, Toshiji</creator><creator>Mori, Yasukiyo</creator><general>S. 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Although aldosterone promotes tissue fibrosis in many organs, its contribution to peritoneal fibrosis and the underlying mechanism are poorly understood. The present study investigated the direct effect of aldosterone on cultured rat peritoneal fibroblasts (RPFs). Methods: The expression of aldosterone synthase (CYP11B2), mineralocorticoid receptors (MRs), 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2), serum- and glucocorticoid-inducible protein kinase 1 (SGK1), and connective tissue growth factor (CTGF) mRNA was evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). To determine the role of reactive oxygen species (ROS) induced by aldosterone, an active oxygen assay with several inhibitors was used. The ability of RPFs to produce aldosterone was examined by enzyme immunoassay. Small interfering RNA (siRNA) of SGK1 was transfected into cultured cells using lipofectamine. Results: CYP11B2, MRs, and 11β-HSD2 were expressed in RPFs. The release of aldosterone from RPFs into the culture medium was confirmed. Aldosterone increased the expression of SGK1 mRNA via ROS generation. Spironolactone, apocynin, and tempol significantly reduced SGK1 expression. Aldosterone upregulated CTGF transcripts significantly. SGK1 gene silencing suppressed aldosterone-induced CTGF expression. Conclusion: The local aldosterone system acts directly as a profibrotic factor via ROS-mediated SGK1 in RPFs.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>19521108</pmid><doi>10.1159/000225379</doi><tpages>9</tpages></addata></record> |
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| subjects | Aldosterone - physiology Animals Cells, Cultured Connective Tissue Growth Factor - biosynthesis Gene Expression Regulation Immediate-Early Proteins - genetics Original Paper Peritoneal Fibrosis - etiology Protein-Serine-Threonine Kinases - genetics Rats Reactive Oxygen Species - metabolism RNA, Messenger - analysis RNA, Small Interfering - pharmacology |
| title | Direct Aldosterone Action as a Profibrotic Factor via ROS-Mediated SGK1 in Peritoneal Fibroblasts |
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