Caveolin-1 deficiency induces premature senescence with mitochondrial dysfunction
- Authors
- Yu, Dong-Min; Jung, Seung Hee; An, Hyoung-Tae; Lee, Sungsoo; Hong, Jin; Park, Jun Sub; Lee, Hyun; Lee, Hwayeon; Bahn, Myeong-Suk; Lee, Hyung Chul; Han, Na-Kyung; Ko, Jesang; Lee, Jae-Seon; Ko, Young-Gyu
- Issue Date
- 8월-2017
- Publisher
- WILEY
- Keywords
- cardiolipin; caveolin-1; mitochondria; senescence; SIRT1
- Citation
- AGING CELL, v.16, no.4, pp.773 - 784
- Indexed
- SCIE
SCOPUS
- Journal Title
- AGING CELL
- Volume
- 16
- Number
- 4
- Start Page
- 773
- End Page
- 784
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/82707
- DOI
- 10.1111/acel.12606
- ISSN
- 1474-9718
- Abstract
- Paradoxical observations have been made regarding the role of cayeolin-1 (Cav-1) during cellular senescence. For example, caveolin-1 deficiency prevents reactive oxygen species-induced cellular senescence despite mitochondrial dysfunction, which leads to senescence. To resolve this paradox, we re addressed the role of caveolin-1 in cellular senescence in human diploid fibroblasts, A549, HCT116, and Cay-1(-/-) mouse embryonic fibroblasts. Cav-1 deficiency (knockout or knockdown) induced cellular senescence via a p53-p21-dependent pathway, downregulating the expression level of the cardiolipin biosynthesis enzymes and then reducing the content of cardiolipin, a critical lipid for mitochondria! respiration. Our results showed that Cav-1 deficiency decreased mitochondrial respiration, reduced the activity of oxidative phosphorylation complex I (CI), inactivated SIRT1, and decreased the NAD(+)/NADH ratio. From these results, we concluded that Cav-1 deficiency induces premature senescence via mitochondrial dysfunction and silent information regulator 2 homologue 1 (SIRT1) inactivation.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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