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首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Receptor tyrosine kinase ligands and inflammatory cytokines cooperatively suppress the fibrogenic activity in temporomandibular-joint-derived fibroblast-like synoviocytes via mitogen-activated protein kinase kinase/extracellular signal-regulated kinase
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Receptor tyrosine kinase ligands and inflammatory cytokines cooperatively suppress the fibrogenic activity in temporomandibular-joint-derived fibroblast-like synoviocytes via mitogen-activated protein kinase kinase/extracellular signal-regulated kinase

机译：受体酪氨酸激酶配体和炎性细胞因子通过丝裂剂活化的蛋白激酶激酶/细胞外信号调节激酶协同抑制颞下颌关节衍生的成纤维细胞样Synociocytes中的纤维化活性

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Osteoarthritis (OA)-related fibrosis is a possible cause of temporomandibular joint (TMJ) stiffness. However, the molecular mechanisms underlying the fibrogenic activity in fibroblast-like synoviocytes (FLSs) remain to be clarified. The present study examined the effects of receptor tyrosine kinase (RTK) ligands, such as fibroblast growth factor (FGF)-1 and epidermal growth factor (EGF), on myofibroblastic differentiation of the FLS cell line FLS1, which is derived from the mouse TMJ. The present study revealed that both FGF-1 and EGF dose-dependently suppressed the expression of the myofibroblast (MF) markers, including α-smooth muscle actin (α-SMA) and type I collagen, in FLS1 cells. Additionally, both FGF-1 and EGF activated extracellular signal-regulated kinase (ERK) in FLS1 cells. In addition, the mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor U0126 abrogated the FGF-1- and EGF-mediated suppression of MF marker expression. On the other hand, inflammatory cytokines, such as interleukin-1β and tumor necrosis factor-α, also suppressed the expression of MF markers in FLS1 cells. Importantly, U0126 abrogated the inflammatory cytokine-mediated suppression of MF marker expression. Interestingly, RTK ligands and inflammatory cytokines additively suppressed the expression of type I collagen. These results suggested that RTK ligands and inflammatory cytokines cooperatively inhibited the fibrogenic activity in FLSs derived from the TMJ in a MEK/ERK-dependent manner. The present findings partially clarify the molecular mechanisms underlying the development of OA-related fibrosis in the TMJ and may aid in identifying therapeutic targets for this condition. Additionally, FGF-1 and EGF could be therapeutically utilized to prevent OA-related fibrosis around the inflammatory TMJ.
机译：骨关节炎（OA） - 相关的纤维化是颞下颌关节（TMJ）刚度的可能原因。然而，仍然澄清成纤维细胞样Synociytes（FLSS）中纤维化活性的分子机制仍然澄清。本研究检测了受体酪氨酸激酶（RTK）配体的影响，例如成纤维细胞生长因子（FGF）-1和表皮生长因子（EGF），衍生自小鼠TMJ的霉菌细胞系分化。本研究表明，FGF-1和EGF剂量依赖性地抑制了肌纤维细胞（MF）标记的表达，包括α-平滑肌肌动蛋白（α-SMA）和I型胶原蛋白，在FLS1细胞中。另外，FGF-1和EGF活化的细胞外信号调节激酶（ERK）在FLS1细胞中。此外，丝裂剂活化的蛋白激酶（MAPK）/ ERK激酶（MEK）抑制剂U0126废除了FGF-1-和EGF介导的MF标志物表达的抑制。另一方面，炎症细胞因子，例如白细胞介素-1β和肿瘤坏死因子-α，也抑制了FLS1细胞中MF标志物的表达。重要的是，U0126废除了MF标志物表达的炎症细胞因子介导的抑制。有趣的是，RTK配体和炎症细胞因子会抑制I型胶原蛋白的表达。这些结果表明RTK配体和炎性细胞因子协同抑制来自梅克/ ERK依赖性的肉体衍生自TMJ的纤维化活性。本研究结果部分阐明了TMJ中综合纤维化的发展潜在的分子机制，并有助于鉴定这种情况的治疗靶标。另外，可以治疗FGF-1和EGF，以防止炎症TMJ周围的OA相关纤维化。

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