Expression and related mechanisms of miR-330-3p and S100B in an animal model of cartilage injury

Abstract

Objective To investigate the roles of and relationship between microRNA (miR)-330-3p and S100 calcium-binding protein B (S100B) in an animal model of cartilage injury. Methods This study included 30 New Zealand male rabbits randomly divided into three groups: an intervention group, a model group and a sham surgery control group. Modelling was performed in the intervention and model groups, but in the sham surgery group, only the skin was cut. After modelling, the intervention and model groups were injected with the miR-330-3p overexpression vector GV268-miR-330-3p or the control GV268-N-ODN vector, respectively, twice a week for 7 weeks. Results Levels of interleukin-1β and tumour necrosis factor-α in the synovial fluid were significantly higher in the model group than in the intervention and control groups. The level of miR-330-3p in the cartilage tissue was significantly higher in the control group than in the model group but it was significantly lower compared with the intervention group. Levels of S100B, fibroblast growth factor receptor 1 and fibroblast growth factor-2 in the cartilage tissue of rabbits in the model group were significantly higher compared with the control and intervention groups. Conclusion These findings demonstrate that the upregulation of miR-330-3p can inhibit the expression of S100B.

Deregulation of exosomal miRNAs in rheumatoid arthritis patients

“…The silencing of gene expression involves either degradation of mRNA or destabilization of transcript resulting in suppression of target protein synthesis [12]. Exosomal miRNA-103a-3p, miRNA-10a-5p, miRNA-204-3p, miRNA-330-3p, and miRNA-19b have been observed deregulated in different diseases and found to be associated with an elevated risk of disease pathogenesis such as cancer [12][13][14][15][16][17][18][19][20][21][22][23]. Deregulation of these microRNAs has also been reported in joint inflammation by targeting different genes such as downregulation of miRNA-10a-5p increases the T-box transcription factor 5 activity and increase the demolition of cartilage [24].…”

“…Wang et al, (2022) has identified the structure-specific recognition protein 1 (Ssrp1) as the target site of the miRNA-204-3p, and deregulation of miRNA-204-3p results in excessive cellular proliferation and synovial inflammation and ultimately leads to RA [27]. Wu et al, (2021) have reported the change in the expression level of miRNA-330-3p in cartilage injury and bone deformities [28]. Previous studies have reported the involvement of miRNA-103a-3p, miRNA-10a-5p, miRNA-204-3p, miRNA-330-3p, and miRNA-19b in synovial PLOS ONE inflammation, cartilage injury, and in inflammatory joint disorder [23][24][25][26][27][28].…”

“…Wu et al, (2021) have reported the change in the expression level of miRNA-330-3p in cartilage injury and bone deformities [28]. Previous studies have reported the involvement of miRNA-103a-3p, miRNA-10a-5p, miRNA-204-3p, miRNA-330-3p, and miRNA-19b in synovial PLOS ONE inflammation, cartilage injury, and in inflammatory joint disorder [23][24][25][26][27][28]. No study has been published concerning involvement of exosomal miRNAs, miRNA-103a-3p, miRNA-10a-5p, miRNA-204-3p, miRNA-330-3p, and miRNA-19b in RA patients.…”