C10orf10/DEPP activates mitochondrial autophagy and maintains chondrocyte viability in the pathogenesis of osteoarthritis
| Autor: | Masanari Kuwahara, Yukio Akasaki, Ichiro Kurakazu, Takuya Sueishi, Masakazu Toya, Taisuke Uchida, Tomoaki Tsutsui, Ryota Hirose, Hidetoshi Tsushima, Takeshi Teramura, Yasuharu Nakashima |
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| Rok vydání: | 2022 |
| Předmět: |
Aged
80 and over Cartilage Articular Male Mice Knockout Cell Death Cell Survival Forkhead Box Protein O3 Intracellular Signaling Peptides and Proteins Middle Aged Biochemistry Mitochondria Mice Inbred C57BL Mice Chondrocytes Osteoarthritis Autophagy Genetics Animals Humans Female Molecular Biology Aged Biotechnology |
| Zdroj: | The FASEB Journal. 36 |
| ISSN: | 1530-6860 0892-6638 |
| Popis: | Osteoarthritis (OA), the most prevalent joint disease, is characterized by the progressive loss of articular cartilage. Autophagy, a lysosomal degradation pathway, maintains cellular homeostasis, and autophagic dysfunction in chondrocytes is a hallmark of OA pathogenesis. However, the cause of autophagic dysfunction in OA chondrocytes remains incompletely understood. Recent studies have reported that decidual protein induced by progesterone (C10orf10/DEPP) positively regulates autophagic functions. In this study, we found that DEPP was involved in mitochondrial autophagic functions of chondrocytes, as well as in OA pathogenesis. DEPP expression decreased in human OA chondrocytes in the absence or presence of pro-inflammatory cytokines, and was induced by starvation, hydrogen peroxide (H |
| Databáze: | OpenAIRE |
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