The DNA repair enzyme apurinic/apyrimidinic endonuclease (Apex Nuclease) 2 has the potential to protect against down-regulation of chondrocyte activity in osteoarthritis
International Journal of Molecular Sciences, ISSN: 1422-0067, Vol: 15, Issue: 9, Page: 14921-14934
2014
- 13Citations
- 7Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef12
- Captures7
- Readers7
Article Description
Apurinic/apyrimidinic endonuclease 2 (Apex 2) plays a critical role in DNA repair caused by oxidative damage in a variety of human somatic cells. We speculated that chondrocyte Apex 2 may protect against the catabolic process of articular cartilage in osteoarthritis (OA). Higher levels of Apex 2 expression were histologically observed in severely compared with mildly degenerated OA cartilage from STR/OrtCrlj mice, an experimental model which spontaneously develops OA. The immunopositivity of Apex 2 was significantly correlated with the degree of cartilage degeneration. Moreover, the OA-related catabolic factor interleukin-1β induced the expression of Apex 2 in chondrocytes, while Apex 2 silencing using small interfering RNA reduced chondrocyte activity in vitro. The expression of Apex 2 in chondrocytes therefore appears to be associated with the degeneration of articular cartilage and could be induced by an OA-related catabolic factor to protect against the catabolic process of articular cartilage. Our findings suggest that Apex 2 may have the potential to prevent the catabolic stress-mediated down-regulation of chondrocyte activity in OA. © 2014 by the authors; licensee MDPI, Basel, Switzerland.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84906826192&origin=inward; http://dx.doi.org/10.3390/ijms150914921; http://www.ncbi.nlm.nih.gov/pubmed/25158232; https://www.mdpi.com/1422-0067/15/9/14921; https://dx.doi.org/10.3390/ijms150914921; http://www.mdpi.com/1422-0067/15/9/14921/; https://www.mdpi.com/1422-0067/15/9/14921/pdf; https://www.mdpi.com/1422-0067/15/9/14921/htm; http://www.mdpi.com/1422-0067/15/9/14921
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