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- Title
25-Hydroxycholesterol-Induced Oxiapoptophagy in L929 Mouse Fibroblast Cell Line.
- Authors
You, Jae-Seek; Lim, HyangI; Seo, Jeong-Yeon; Kang, Kyeong-Rok; Kim, Do Kyung; Oh, Ji-Su; Seo, Yo-Seob; Lee, Gyeong-Je; Kim, Jin-Soo; Kim, Heung-Joong; Yu, Sun-Kyoung; Kim, Jae-Sung
- Abstract
25-hydroxycholesterol (25-HC) is an oxysterol synthesized from cholesterol by cholesterol-25-hydroxylase during cholesterol metabolism. The aim of this study was to verify whether 25-HC induces oxiapoptophagy in fibroblasts. 25-HC not only decreased the survival of L929 cells, but also increased the number of cells with condensed chromatin and altered morphology. Fluorescence-activated cell sorting results showed that there was a dose-dependent increase in the apoptotic populations of L929 cells upon treatment with 25-HC. 25-HC-induced apoptotic cell death was mediated by the death receptor-dependent extrinsic and mitochondria-dependent intrinsic apoptosis pathway, through the cascade activation of caspases including caspase-8, -9, and -3 in L929 cells. There was an increase in the levels of reactive oxygen species and inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in L929 cells treated with 25-HC. Moreover, 25-HC caused an increase in the expression of beclin-1 and microtubule-associated protein 1A/1B-light chain 3, an autophagy biomarker, in L929 cells. There was a significant decrease in the phosphorylation of protein kinase B (Akt) in L929 cells treated with 25-HC. Taken together, 25-HC induced oxiapoptophagy through the modulation of Akt and p53 cellular signaling pathways in L929 cells.
- Subjects
CELL death; INFLAMMATORY mediators; CELL populations; PROTEIN kinase B; NITRIC-oxide synthases; FIBROBLASTS; HYDROXYCHOLESTEROLS; DEATH receptors
- Publication
Molecules, 2022, Vol 27, Issue 1, p199
- ISSN
1420-3049
- Publication type
Article
- DOI
10.3390/molecules27010199