p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction
Mitochondrial dysfunction is increasingly recognized as an important factor in glomerular diseases. Previous study has shown that mitochondrial fission contributed to mitochondrial dysfunction. However, the mechanism of mitochondrial fission on mitochondrial dysfunction in aldosterone-induced podocy...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2018-05, Vol.314 (5), p.F798-F808 |
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| container_issue | 5 |
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| container_title | American journal of physiology. Renal physiology |
| container_volume | 314 |
| creator | Yuan, Yanggang Zhang, Aiqing Qi, Jia Wang, Hui Liu, Xi Zhao, Min Duan, Suyan Huang, Zhimin Zhang, Chengning Wu, Lin Zhang, Bo Zhang, Aihua Xing, Changying |
| description | Mitochondrial dysfunction is increasingly recognized as an important factor in glomerular diseases. Previous study has shown that mitochondrial fission contributed to mitochondrial dysfunction. However, the mechanism of mitochondrial fission on mitochondrial dysfunction in aldosterone-induced podocyte injury remains ambiguous. This study aimed to investigate the pathogenic effect of mitochondrial fission both in vivo and in vitro. In an animal model of aldosterone-induced nephropathy, inhibition of the mitochondrial fission protein dynamin-related protein 1 (Drp1) suppressed aldosterone-induced podocyte injury. In cultured podocytes, aldosterone dose dependently induced Drp1 expression. Knockdown of Drp1 inhibited aldosterone-induced mitochondrial fission, mitochondrial dysfunction, and podocyte apoptosis. Furthermore, aldosterone dose dependently induced p53 expression. Knockdown of p53 inhibited aldosterone-induced Drp1 expression, mitochondrial dysfunction, and podocyte apoptosis. These findings implicated that aldosterone induced mitochondrial dysfunction and podocyte injury mediated by p53/Drp1-dependent mitochondrial fission, which may provide opportunities for therapeutic intervention for podocyte injury. |
| doi_str_mv | 10.1152/ajprenal.00055.2017 |
| format | Article |
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Previous study has shown that mitochondrial fission contributed to mitochondrial dysfunction. However, the mechanism of mitochondrial fission on mitochondrial dysfunction in aldosterone-induced podocyte injury remains ambiguous. This study aimed to investigate the pathogenic effect of mitochondrial fission both in vivo and in vitro. In an animal model of aldosterone-induced nephropathy, inhibition of the mitochondrial fission protein dynamin-related protein 1 (Drp1) suppressed aldosterone-induced podocyte injury. In cultured podocytes, aldosterone dose dependently induced Drp1 expression. Knockdown of Drp1 inhibited aldosterone-induced mitochondrial fission, mitochondrial dysfunction, and podocyte apoptosis. Furthermore, aldosterone dose dependently induced p53 expression. Knockdown of p53 inhibited aldosterone-induced Drp1 expression, mitochondrial dysfunction, and podocyte apoptosis. These findings implicated that aldosterone induced mitochondrial dysfunction and podocyte injury mediated by p53/Drp1-dependent mitochondrial fission, which may provide opportunities for therapeutic intervention for podocyte injury.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00055.2017</identifier><identifier>PMID: 28659272</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Aldosterone ; Apoptosis ; Dynamin ; Mitochondria ; Nephropathy ; p53 Protein ; Proteins</subject><ispartof>American journal of physiology. 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Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Mitochondrial dysfunction is increasingly recognized as an important factor in glomerular diseases. Previous study has shown that mitochondrial fission contributed to mitochondrial dysfunction. However, the mechanism of mitochondrial fission on mitochondrial dysfunction in aldosterone-induced podocyte injury remains ambiguous. This study aimed to investigate the pathogenic effect of mitochondrial fission both in vivo and in vitro. In an animal model of aldosterone-induced nephropathy, inhibition of the mitochondrial fission protein dynamin-related protein 1 (Drp1) suppressed aldosterone-induced podocyte injury. In cultured podocytes, aldosterone dose dependently induced Drp1 expression. Knockdown of Drp1 inhibited aldosterone-induced mitochondrial fission, mitochondrial dysfunction, and podocyte apoptosis. Furthermore, aldosterone dose dependently induced p53 expression. Knockdown of p53 inhibited aldosterone-induced Drp1 expression, mitochondrial dysfunction, and podocyte apoptosis. These findings implicated that aldosterone induced mitochondrial dysfunction and podocyte injury mediated by p53/Drp1-dependent mitochondrial fission, which may provide opportunities for therapeutic intervention for podocyte injury.</description><subject>Aldosterone</subject><subject>Apoptosis</subject><subject>Dynamin</subject><subject>Mitochondria</subject><subject>Nephropathy</subject><subject>p53 Protein</subject><subject>Proteins</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpdkctKxDAUQIMovr9AkIIbNx1z85p2Kb5hwI2Cu5BJbjFDJ6lJu5i_N-Nr4SqBnHsI9xByBnQGINmVWQ0Jg-lnlFIpZ4zCfIcclhdWg1Bqt9xbDnUj528H5CjnVeEAGOyTA9Yo2bI5OyR5kPzqNg1QOxwwOAxjtfZjtO8xuORNX3U-Zx9DtUbnzYi5Mr2LecQUA9Y-uMmiq4boot2MWPmwmtKmMsH907hN7qZgx6I6IXud6TOe_pzH5PX-7uXmsV48PzzdXC9qK4QYa8kb24CyS-iE4qaTCGxOy68lcG4bJoxC4ZhaKtdSA6JQjEvWQYdcLQXjx-Ty2zuk-DFhHvXaZ4t9bwLGKWtoQTRC0VYW9OIfuopTKsvNmtGGtoWkWyH_pmyKOSfs9JD82qSNBqq3TfRvE_3VRG-blKnzH_e0LEv8m_mNwD8Bn4qKzA</recordid><startdate>20180501</startdate><enddate>20180501</enddate><creator>Yuan, Yanggang</creator><creator>Zhang, Aiqing</creator><creator>Qi, Jia</creator><creator>Wang, Hui</creator><creator>Liu, Xi</creator><creator>Zhao, Min</creator><creator>Duan, Suyan</creator><creator>Huang, Zhimin</creator><creator>Zhang, Chengning</creator><creator>Wu, Lin</creator><creator>Zhang, Bo</creator><creator>Zhang, Aihua</creator><creator>Xing, Changying</creator><general>American Physiological Society</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20180501</creationdate><title>p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction</title><author>Yuan, Yanggang ; Zhang, Aiqing ; Qi, Jia ; Wang, Hui ; Liu, Xi ; Zhao, Min ; Duan, Suyan ; Huang, Zhimin ; Zhang, Chengning ; Wu, Lin ; Zhang, Bo ; Zhang, Aihua ; Xing, Changying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-538c816cb1f463af5e12702725133c824a6e4d26b6d90a14f462352f1fe36b423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aldosterone</topic><topic>Apoptosis</topic><topic>Dynamin</topic><topic>Mitochondria</topic><topic>Nephropathy</topic><topic>p53 Protein</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Yanggang</creatorcontrib><creatorcontrib>Zhang, Aiqing</creatorcontrib><creatorcontrib>Qi, Jia</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Liu, Xi</creatorcontrib><creatorcontrib>Zhao, Min</creatorcontrib><creatorcontrib>Duan, Suyan</creatorcontrib><creatorcontrib>Huang, Zhimin</creatorcontrib><creatorcontrib>Zhang, Chengning</creatorcontrib><creatorcontrib>Wu, Lin</creatorcontrib><creatorcontrib>Zhang, Bo</creatorcontrib><creatorcontrib>Zhang, Aihua</creatorcontrib><creatorcontrib>Xing, Changying</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Yanggang</au><au>Zhang, Aiqing</au><au>Qi, Jia</au><au>Wang, Hui</au><au>Liu, Xi</au><au>Zhao, Min</au><au>Duan, Suyan</au><au>Huang, Zhimin</au><au>Zhang, Chengning</au><au>Wu, Lin</au><au>Zhang, Bo</au><au>Zhang, Aihua</au><au>Xing, Changying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2018-05-01</date><risdate>2018</risdate><volume>314</volume><issue>5</issue><spage>F798</spage><epage>F808</epage><pages>F798-F808</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Mitochondrial dysfunction is increasingly recognized as an important factor in glomerular diseases. Previous study has shown that mitochondrial fission contributed to mitochondrial dysfunction. However, the mechanism of mitochondrial fission on mitochondrial dysfunction in aldosterone-induced podocyte injury remains ambiguous. This study aimed to investigate the pathogenic effect of mitochondrial fission both in vivo and in vitro. In an animal model of aldosterone-induced nephropathy, inhibition of the mitochondrial fission protein dynamin-related protein 1 (Drp1) suppressed aldosterone-induced podocyte injury. In cultured podocytes, aldosterone dose dependently induced Drp1 expression. Knockdown of Drp1 inhibited aldosterone-induced mitochondrial fission, mitochondrial dysfunction, and podocyte apoptosis. Furthermore, aldosterone dose dependently induced p53 expression. Knockdown of p53 inhibited aldosterone-induced Drp1 expression, mitochondrial dysfunction, and podocyte apoptosis. These findings implicated that aldosterone induced mitochondrial dysfunction and podocyte injury mediated by p53/Drp1-dependent mitochondrial fission, which may provide opportunities for therapeutic intervention for podocyte injury.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>28659272</pmid><doi>10.1152/ajprenal.00055.2017</doi><oa>free_for_read</oa></addata></record> |
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| source | American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aldosterone Apoptosis Dynamin Mitochondria Nephropathy p53 Protein Proteins |
| title | p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction |
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