首页> 美国卫生研究院文献>Aging (Albany NY) >Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression
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Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression

机译:取决于通过还原miR-320a表达增加人骨关节炎滑膜成纤维细胞中的ICAM-1表达和单核细胞粘附性

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摘要

Pathophysiological events that modulate the progression of structural changes in osteoarthritis (OA) include monocyte adhesion and infiltration, and synovial inflammation. In particular, the adhesion protein intercellular adhesion molecule type 1 (ICAM-1) promotes monocyte recruitment into the synovial tissue. Visfatin is an adipocyte hormone that promotes the release of inflammatory cytokines during OA progression. We report that visfatin enhances ICAM-1 expression in human OA synovial fibroblasts (OASFs) and facilitates the adhesion of monocytes with OASFs. AMPK and p38 inhibitors, as well as their respective siRNAs, attenuated the effects of visfatin upon ICAM-1 synthesis and monocyte adhesion. We also describe how miR-320a negatively regulates visfatin-induced promotion of ICAM-1 expression and monocyte adhesion. We detail how visfatin affects ICAM-1 expression and monocyte adhesion with OASFs by inhibiting miR-320a synthesis via the AMPK and p38 signaling pathways.
机译:调节骨关节炎(OA)结构变化进展的病理生理事件包括单核细胞粘附和浸润,以及滑膜炎症。特别地,粘附蛋白细胞间粘附分子1(ICAM-1)促进单核细胞募集到滑膜组织中。 visfatin是一种脂肪细胞激素,可在OA进展期间促进炎症细胞因子的释放。我们报告,取磷在人OA滑膜成纤维细胞(OASF)中增强了ICAM-1表达,并促进单核细胞与OASF的粘附性。 AMPK和P38抑制剂以及它们各自的SIRNA,减弱了粘霉素对ICAM-1合成和单核细胞粘附的影响。我们还描述了MIR-320A如何负调节visfatin诱导的ICAM-1表达和单核细胞粘附的促进。我们通过通过AMPK和P38信号传导途径抑制miR-320a合成,详细介绍了visfatin如何通过抑制miR-320a合成来利用OASF来影响oasfs的单核细胞粘附。

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