激活素 A 和 TNF-α 通过 Smad3 非依赖信号通路对 L929 成纤维细胞激活的拮抗作用。
Antagonistic effects of activin A and TNF-α on the activation of L929 fibroblast cells via Smad3-independent signaling.
机构信息
Department of Immunology, College of Basic Medical Sciences, Jilin University, 126 Xinmin Street, Changchun, 130021, Jilin, China.
Department of General Dentistry, School and Hospital of Stomatology, Jilin University, Changchun, 130021, Jilin, China.
出版信息
Sci Rep. 2020 Nov 26;10(1):20623. doi: 10.1038/s41598-020-77783-8.
Fibroblasts play an important role in inflammation and tissue fibrosis. Both activin A and TNF-α can activate immune cells, however, the roles and relationship of them in activating fibroblasts in inflammation remain unclear. Here, this study revealed that TNF-α promoted the release of NO and IL-6 by L929 fibroblast cells, but co-treatment with activin A attenuated these effects. In contrast, activin A induced cell migration and increased the production of tissue fibrosis-related TGF-β1 and fibronectin, while TNF-α inhibited these function changes of L929 cells induced by activin A. Moreover, this study revealed that activin A and TNF-α regulated the activities of L929 cells via ERK1/2/MAPK pathway, rather than Smad3-dependent signaling pathway. Taken together, these data indicate that activin A and TNF-α exert mutually antagonistic effects on regulating fibroblasts activities, and the balance between their action may determine the process and outcome of fibroblasts-mediated inflammation.
成纤维细胞在炎症和组织纤维化中起着重要作用。激活素 A 和 TNF-α 均可激活免疫细胞,但它们在炎症中激活成纤维细胞的作用和关系尚不清楚。本研究揭示,TNF-α 促进了 L929 成纤维细胞释放 NO 和 IL-6,但与激活素 A 共同处理则减弱了这些作用。相反,激活素 A 诱导细胞迁移并增加组织纤维化相关 TGF-β1 和纤维连接蛋白的产生,而 TNF-α 抑制了激活素 A 诱导的 L929 细胞的这些功能变化。此外,本研究揭示,激活素 A 和 TNF-α 通过 ERK1/2/MAPK 途径调节 L929 细胞的活性,而不是 Smad3 依赖性信号通路。总之,这些数据表明,激活素 A 和 TNF-α 对调节成纤维细胞活性具有相互拮抗的作用,它们作用的平衡可能决定了成纤维细胞介导的炎症的过程和结果。
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