ArticlePloS one2024
Dehydroepiandrosterone inhibits ADAMTS expression via an ERK-dependent mechanism in chondrocytes.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Immune dynamics throughout life in relation to sex hormones and perspectives gained from gender-affirming hormone therapy.Frontiers in immunology · 2024Review
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5 authors.
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Abstract
Osteoarthritis (OA) is a joint disease in which cartilage degradation is the hallmark pathological change. In this study, we investigated the anti-osteoarthritic effects of DHEA in rabbit chondrocytes. Polymerase chain reaction was performed to evaluate the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, ADAMTS-5, aggrecan and collagen type 2. In addition, ERK1/2 signaling pathway components were analyzed by Western blotting. In IL-1β-induced chondrocytes, the phosphorylation of ERK1/2 was enhanced, and the downstream catabolic genes, including ADAMTS-4 and ADAMTS-5, were upregulated, while the anabolic genes aggrecan and collagen type 2 were downregulated. DHEA administration restored the IL-1β-induced imbalance in anabolic and catabolic gene expression. In addition, the phosphorylation of ERK1/2 was suppressed by DHEA. Then, PD98059 was used to block the ERK1/2 signaling pathway. The protective effect of DHEA was significantly increased when ERK1/2 signaling was inactivated. DHEA may exert its protective effect by suppressing ADAMTS in an ERK1/2-dependent manner in rabbit chondrocytes.
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