Abstract
This research aimed to explore the role of period circadian clock 2 (Per2) in the evolution of osteoarthritis (OA) and the relevant mechanisms. Per2 messenger RNA (mRNA) and protein levels were markedly reduced in NHAC-kn cells treated with 5 µg/ml lipopolysaccharide (LPS) for 12 h. Then, pcDNA3.1-Per2 and si-Per2 were recruited to boost and reduce the expression of Per2, respectively. MTT assay, apoptosis analysis and enzyme-linked immunosorbent assay (ELISA) results showed that Per2 increased cell proliferation, while inhibited apoptosis and inflammation. Furthermore, the PTEN/PI3K/Akt signalling pathway was activated by Per2 overexpression; the CO-IP data confirmed that Per2 specifically bound to PTEN. Through employing IGF-1, a PI3K activator, we determined that Per2-mediated inflammation response in LPS-stimulated NHAC-kn cells through the PTEN/PI3K/Akt signalling pathway. In summary, the present study indicates that Per2 may serve as a novel therapeutic target through activating the PTEN/PI3K/Akt signalling pathway.
Highlights
Osteoarthritis (OA), a kind of chronic degenerative joint disease, is prevalent among the elderly
Period circadian clock 2 (Per2) messenger RNA (mRNA) and protein expression were significantly decreased in NHAC-kn cells after 5 and 10 μg/ml LPS treatment for 12 h compared with untreated cells (Figure 1A,B)
Per2 is related to inflammation response, like myocardial inflammation [31] and dermatitis [32]
Summary
Osteoarthritis (OA), a kind of chronic degenerative joint disease, is prevalent among the elderly. Circadian genes are imperative regulators of immune function [5]. Existing research has demonstrated that circadian clock genes influence some downstream genes in cartilage tissue and, in turn, participate in related diseases [6]. These genes affect endochondral ossification, and there is circadian variation in chondrocyte proliferation and the change rate of growth plates [7]. Period circadian clock 2 (Per2) participates in inhibiting tumours via targeting other genes that are relevant to cell proliferation and death, including cyclin A1, transformed mouse 3T3 cell double minute 2 and cyclin-dependent kinase 1 [8,9]. The effects of Per on the development of OA are not yet clear
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