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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| Published in | American journal of physiology. Renal physiology Vol. 314; no. 5; pp. F798 - F808 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
American Physiological Society
01.05.2018
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| 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. |
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| AbstractList | 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. 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.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. |
| Author | Xing, Changying Zhang, Aiqing Yuan, Yanggang Wang, Hui Duan, Suyan Zhao, Min Zhang, Chengning Zhang, Aihua Liu, Xi Qi, Jia Zhang, Bo Huang, Zhimin Wu, Lin |
| Author_xml | – sequence: 1 givenname: Yanggang surname: Yuan fullname: Yuan, Yanggang organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 2 givenname: Aiqing surname: Zhang fullname: Zhang, Aiqing organization: Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 3 givenname: Jia surname: Qi fullname: Qi, Jia organization: Department of Pharmacy, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China – sequence: 4 givenname: Hui surname: Wang fullname: Wang, Hui organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 5 givenname: Xi surname: Liu fullname: Liu, Xi organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 6 givenname: Min surname: Zhao fullname: Zhao, Min organization: Department of Nephrology, Nanjing Children's Hospital, Nanjing Medical University, Nanjing, China – sequence: 7 givenname: Suyan surname: Duan fullname: Duan, Suyan organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 8 givenname: Zhimin surname: Huang fullname: Huang, Zhimin organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 9 givenname: Chengning surname: Zhang fullname: Zhang, Chengning organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 10 givenname: Lin surname: Wu fullname: Wu, Lin organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 11 givenname: Bo surname: Zhang fullname: Zhang, Bo organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China – sequence: 12 givenname: Aihua surname: Zhang fullname: Zhang, Aihua organization: Department of Nephrology, Nanjing Children's Hospital, Nanjing Medical University, Nanjing, China – sequence: 13 givenname: Changying surname: Xing fullname: Xing, Changying organization: Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China |
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| SubjectTerms | Aldosterone Aldosterone - administration & dosage Aldosterone - toxicity Animals Apoptosis Apoptosis - drug effects Cell Line Dose-Response Relationship, Drug Dynamin Dynamins - genetics Dynamins - metabolism Infusions, Subcutaneous Kidney Diseases - chemically induced Kidney Diseases - metabolism Kidney Diseases - pathology Kidney Diseases - prevention & control Male Mice, Inbred C57BL Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondria - pathology Mitochondrial Dynamics - drug effects Nephropathy p53 Protein Podocytes - drug effects Podocytes - metabolism Podocytes - pathology Proteins Quinazolinones - pharmacology Signal Transduction - drug effects Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| Title | p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction |
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