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

Abstract

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