Key Laboratory of Microecology-Immunomodulatory Network and Related Diseases, School of Basic Medical Sciences, Jiamusi University, Jiamusi 154000, Heilongjiang Province, PR China; Jiamusi University Affiliated Stomatological Hospital, Heilongjiang Key Laboratory of Oral Biomedical Materials and Clinical Application, Jiamusi 154000, Heilongjiang Province, PR China; Shandong Key Laboratory of Oral Tissue Regeneration, School of Dentistry, Shandong University, Jinan 250100, Shandong Province, PR China.
Beijing Citident Hospital of Stomatology, Beijing 100032, PR China; Beijing Implant Training College, Beijing 100032, PR China.
Arch Oral Biol. 2022 Oct;142:105511. doi: 10.1016/j.archoralbio.2022.105511. Epub 2022 Jul 16.
This study aimed to investigate the role of miR-132-3p in the progression of temporomandibular joint osteoarthritis (TMJOA) and its potential pathological mechanism.
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.
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.
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.
本研究旨在探讨 miR-132-3p 在颞下颌关节骨关节炎（TMJOA）进展中的作用及其潜在的病理机制。
采用单侧前牙反𬌗法建立 6 只大鼠 TMJOA 模型。通过 miRNA 测序检测 TMJOA（n=6）和对照组（n=6）中 miR-132-3p 的差异表达，并通过 PCR 验证。体外培养髁突软骨细胞，用 IL-1β 刺激模拟 TMJOA。上调 miR-132-3p 表达后，检测这些软骨细胞的增殖、凋亡、炎症和细胞外基质的变化。验证 miR-132-3p 与 TMJOA 中 PTEN 的靶向关系，并通过同时上调 miR-132-3p 和 PTEN 的表达进行挽救实验。
与对照组相比，TMJOA 大鼠软骨组织和 IL-1β 诱导的 TMJ 软骨细胞中 miR-132-3p 表达降低。上调 miR-132-3p 表达后，IL-1β 诱导的 TMJ 软骨细胞的细胞增殖活性和聚集蛋白聚糖及 II 型胶原的表达水平增加，凋亡率和炎症因子水平降低。miR-132-3p 可以靶向调控 PTEN 的表达，上调 PTEN 表达可以逆转 miR-132-3p 表达上调对 TMJOA 细胞的影响。
miR-132-3p 在 TMJOA 中表达下调，通过靶向调控 PTEN，调节 TMJOA 软骨细胞的增殖、细胞外基质和炎症反应，参与 TMJOA 的进展。
