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<p>MicroRNA140-5p has been implicated in temporomandibular joint osteoarthritis (TMJ-OA), though its precise mechanistic role remains unclear. This study investigates the molecular mechanisms underlying microRNA140-5p-mediated inflammatory responses in TMJ-OA. In vitro, mandibular condylar chondrocytes (MCCs) were treated with IL-1β and transfected with small interfering RNA (siRNA) targeting Smad3, a direct target of microRNA140-5p. Expression of inflammatory cytokines was assessed via Western blotting and RT-qPCR. In vivo, a TMJ-OA model was established in Sprague–Dawley (SD) rats, followed by intra-articular injection of antagomir140-5p into the superior joint cavity. Histopathological and immunohistochemical (IHC) analyses were performed using hematoxylin–eosin (HE) staining. Our findings demonstrate that IL-1β treatment upregulated microRNA140-5p expression in MCCs. Overexpression of microRNA140-5p suppressed chondrocyte proliferation and cartilage formation while promoting apoptosis. Conversely, antagomir140-5p administration preserved cartilage integrity in TMJ-OA, restoring expression of SOX9, COL2A1, SMAD3, and TGF-β3, while suppressing inflammatory mediators such as RUNX2 and NF-κB. These findings suggest that the abnormal expression of microRNA-140-5p in condylar cartilage may reflect the pathological progression of temporomandibular joint osteoarthritis, with its potential mechanism likely mediated through regulation of the TGF-β/SMAD/SOX/NF-κB signaling axis.</p>

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Signaling network exploration of microRNA140-5p in response to TMJ-OA pathological changes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月22日

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  • Weihao Li,
  • Jun Zhang,
  • Sihang Li,
  • Jianzhong Chen

摘要

MicroRNA140-5p has been implicated in temporomandibular joint osteoarthritis (TMJ-OA), though its precise mechanistic role remains unclear. This study investigates the molecular mechanisms underlying microRNA140-5p-mediated inflammatory responses in TMJ-OA. In vitro, mandibular condylar chondrocytes (MCCs) were treated with IL-1β and transfected with small interfering RNA (siRNA) targeting Smad3, a direct target of microRNA140-5p. Expression of inflammatory cytokines was assessed via Western blotting and RT-qPCR. In vivo, a TMJ-OA model was established in Sprague–Dawley (SD) rats, followed by intra-articular injection of antagomir140-5p into the superior joint cavity. Histopathological and immunohistochemical (IHC) analyses were performed using hematoxylin–eosin (HE) staining. Our findings demonstrate that IL-1β treatment upregulated microRNA140-5p expression in MCCs. Overexpression of microRNA140-5p suppressed chondrocyte proliferation and cartilage formation while promoting apoptosis. Conversely, antagomir140-5p administration preserved cartilage integrity in TMJ-OA, restoring expression of SOX9, COL2A1, SMAD3, and TGF-β3, while suppressing inflammatory mediators such as RUNX2 and NF-κB. These findings suggest that the abnormal expression of microRNA-140-5p in condylar cartilage may reflect the pathological progression of temporomandibular joint osteoarthritis, with its potential mechanism likely mediated through regulation of the TGF-β/SMAD/SOX/NF-κB signaling axis.