Abstract
As a common joint disease, osteoarthritis exhibits increasing trend in recent years. C-X-C motif chemokine receptor 3 (CXCR3) is a kind of chemokine with the characteristic of recruiting inflammatory cells. Its function in osteoarthritis has not been clarified. This study aims to explore the role of CXCR3 in cartilage injury by affecting unfolded protein response (UPR) pathway. The sample was obtained from osteoarthritis patients to test CXCR3 expression by Real-time polymerase chain reaction (PCR). Chondrocyte apoptosis model was established in vitro induced by interleukin 1β (IL-1β) and sodium nitroprusside (SNP). CXCR3 level was downregulated by using siRNA. Cell apoptosis was determined by using transferase-mediated deoxyuridine triphosphate-biotin nick end labeling(TUNEL) assay. UPR pathway related factors C/EBP homology protein (CHOP) and glucose regulated protein78 (GRP78) protein expressions were tested by using Western blot. CXCR3 protein level significantly increased in osteoarthritis patients (2.66 ± 0.25 vs. 1.00 ± 0.05, p<0.05). CXCR3 siRNA significantly reduced nitrate level in chondrocytes induced by IL-β (35.22 ± 1.76 vs. 17.82 ± 0.89, p<0.05) without affecting cell apoptosis (1.13 ± 0.05 vs. 0.859 ± 0.04, p>0.05). CXCR3 siRNA markedly downregulated nitrate level in chondrocytes (50.63 ± 2.53 vs. 30.63 ± 1.63, p<0.05) and alleviated cell apoptosis induced by SNP (1.98 ± 0.10 vs. 1.25 ± 0.06, p<0.05). UPR pathway C/EBP homology protein (CHOP) and glucose regulated protein78 (GRP78) participated in the process of chondrocyte apoptosis. Endoplasmic reticulum (ER) stress signaling pathway CHOP and GRP78 are involved in CXCR3 receptor attenuating chondrocyte apoptosis induced by SNP.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: European review for medical and pharmacological sciences
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
