Inhibition of LncRNA SNHG14 protects chondrocyte from injury in osteoarthritis via sponging miR-137

Abstract

Long-chain noncoding small nucleolar RNA host gene 14 (LncRNA SNHG14) is highly expressed in various diseases and promotes diseases progression, but the role and mechanism of LncRNA SNHG14 on targeting miR-137 in promoting osteoarthritis (OA) chondrocyte injury remains unclear. To measure the expression of the LncRNAs SNHG14 and miR-137, cell survival, inflammatory response, chondrocyte apoptosis, and extracellular matrix (ECM) levels, we subjected human chondrocytes to a variety of lipopolysaccharide (LPS) concentrations. To measure the luciferase activity of SNHG14-WT and SNHG14-MUT transfected with miR-137 mimic or miR-NC mimic, luciferase reporter genes were utilized. The results showed that chondrocyte viability was significantly inhibited with LPS treatment and chondrocyte inflammatory response, apoptosis and extracellular matrix degradation were significantly increased. However, the above results were significantly reversed after LncRNA SNHG14 inhibition. The luciferase activity bound to miR-137 was decreased in SNHG14-WT group, but there was no change in SNHG14-mut group, which indicated that LncRNA SNHG14 inhibited miR-137 expression as a miRNA sponge. In conclusion, inhibition of LncRNA SNHG14 attenuates chondrocyte inflammatory response, apoptosis and extracellular matrix degradation by targeting miR-137 in LPS induced chondrocytes.

Keywords:

• LncRNA SNHG14
• osteoarthritis
• inflammation
• extracellular matrix degradation
• apoptosis

Acknowledgments

We want to thanks JSJ for giving suggestions.

Authors’ contributions

ZD and XC contributed to the conception and design of the study. CT and LSW carried out the principal experiments. WLL and YKY contributed to the analysis and interpretation of the data. XC contributed to the drafting of the article. JCG contributed to the critical revision of important intellectual content. All authors read and approved the final manuscript.

Consent for publication

Not applicable.

Conflicts of interest

The authors declare that they are free from conflict of interest in presenting it.

Data availability

The datasets used in the present study are available from the corresponding authors on reasonable request.

Additional information

Funding

This work was supported by grants from the Changzhou Science & Technology Program (Grant No. CJ20220125 to D.Z.), the Changzhou Science and Technology Bureau (WZ202204 to C.X.), Changzhou No. 2. People’s Hospital Foundation (2022K004 to C.X.).