ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2014
Involvement of ERCC1 in the pathogenesis of osteoarthritis through the modulation of apoptosis and cellular senescence.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- An Integrated View of Stressors as Causative Agents in OA Pathogenesis.Biomolecules · 2023Review
- Integrating transcriptome-wide association study and mRNA expression profile identified candidate genes related to hand osteoarthritis.Arthritis research & therapy · 2021Article
- Influence of swimming exercise on the expression of apoptotic gene caspase-3 in chondrocytes in osteoarthritis.American journal of translational research · 2021Article
- Deficiency in the DNA repair protein ERCC1 triggers a link between senescence and apoptosis in human fibroblasts and mouse skin.Aging cell · 2020Article
- OPN Deficiency Increases the Severity of Osteoarthritis Associated with Aberrant Chondrocyte Senescence and Apoptosis and Upregulates the Expression of Osteoarthritis-Associated Genes.Pain research & management · 2020Article
- Ageing and the pathogenesis of osteoarthritis.Nature reviews. Rheumatology · 2016Review
- Call for standardized definitions of osteoarthritis and risk stratification for clinical trials and clinical use.Osteoarthritis and cartilage · 2015Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
DNA damage is a cause of age related pathologies, including osteoarthritis (OA). Excision repair cross complementation group 1 (ERCC1) is an endonuclease required for DNA damage repair. In this study we investigated the function of ERCC1 in chondrocytes and its association with the pathophysiology of OA. ERCC1 expression in normal and osteoarthritic cartilage was assessed, as were changes in ERCC1 expression in chondrocytes under catabolic stress. Inhibiting ERCC1 in chondrocytes under interleukin-1β stimulation using small interfering RNA (siRNA) was also evaluated. Finally, cellular senescence and apoptosis were examined in relation to ERCC1 function. ERCC1 expression was decreased in OA cartilage and increased within 4 h of exposure to interleukin (IL)-1β, but decreased after 12 h. The inhibition of ERCC1 by siRNA increased the expression of matrix metallopeptidase 13 and decreased collagen type II. ERCC1 inhibition also increased the number of apoptotic and senescent cells. The inhibition of ERCC1 in chondrocytes increased their expression of OA related proteins, apoptosis, cellular senescence, and hypertrophic-like changes which suggest that ERCC1 is critical for protecting human chondrocytes (HCs) from catabolic stresses and provides insights into the pathophysiology of OA and a potential target for its treatment. (191)
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Registered trials
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