miR-132-3p participates in the pathological mechanism of temporomandibular joint osteoarthritis by targeting PTEN.

OBJECTIVE

This study aimed to investigate the role of miR-132-3p in the progression of temporomandibular joint osteoarthritis (TMJOA) and its potential pathological mechanism.

DESIGN

A TMJOA model was established using six rats via the unilateral anterior crossbite method. The differential expression of miR-132-3p in the TMJOA (n = 6) and control groups (n = 6) was detected via miRNA sequencing and verified via PCR. The chondrocytes in the condylar cartilage of the temporomandibular joint were cultured and stimulated with IL-1β to simulate TMJOA in vitro. The changes in the proliferation, apoptosis, inflammation and extracellular matrix of these chondrocytes were detected after the upregulation of miR-132-3p expression. The targeted relationship of miR-132-3p and PTEN in TMJOA was verified, and rescue experiments were conducted via co-upregulation of the expression of both miR-132-3p and PTEN.

RESULTS

Compared with that in the control group, miR-132-3p expression was lower in the cartilage tissues of TMJOA rats and IL-1β-induced TMJ chondrocytes. After upregulating the expression of miR-132-3p, the cell proliferation activity and expression levels of aggrecan and type II collagen of IL-1β-induced TMJ chondrocytes were increased, and the apoptosis rate and levels of inflammatory factors were decreased. miR-132-3p can regulate PTEN expression in a targeted manner, and upregulating PTEN expression could reverse the influences of the upregulation of miR-132-3p expression on TMJOA cells.

CONCLUSION

miR-132-3p is less expressed in TMJOA, and it regulates the proliferation, extracellular matrix, and inflammatory response of TMJOA chondrocytes and participates in TMJOA progression by targeting PTEN.