SPRED2 promotes autophagy and attenuates inflammatory response in IL-1β induced osteoarthritis chondrocytes via regulating the p38 MAPK signaling pathway

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell Pub Date : 2023-06-01 DOI:10.1016/j.tice.2023.102086

Jie Wei , Guopeng You , Hongjuan Cheng , Chen Gao

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引用次数: 1

Abstract

Osteoarthritis (OA) is an age-related degenerative disease primarily characterized by articular cartilage degeneration. Many inflammatory mediators are upregulated in OA patients. Mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways play a role in the regulation of inflammatory response. Autophagy appears to exhibit a protective mechanism, and alleviate the symptoms of OA in rats. Dysregulation of SPRED2 is associated with various diseases involving inflammatory response. However, the role of SPRED2 in OA development remains to be investigated. The present work demonstrated that SPRED2 promoted autophagy and attenuated inflammatory response in IL-1β induced osteoarthritis chondrocytes via regulating the p38 MAPK signaling pathway. SPRED2 was downregulated in human knee cartilage tissues of OA patients and in IL-1β-induced chondrocytes. SPRED2 enhanced chondrocyte proliferation and prevented cell apoptosis induced by IL-1β. SPRED2 prevented IL-1β-induced chondrocytes autophagy and inflammatory response in chondrocytes. SPRED2 inhibited the activation of p38 MAPK signaling pathway and ameliorated OA injury of cartilage. Thus, SPRED2 promoted autophagy and inhibited inflammatory response by regulation of p38 MAPK signaling pathway in vivo.

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SPRED2通过调节p38 MAPK信号通路促进IL-1β诱导的骨关节炎软骨细胞的自噬和减轻炎症反应

骨关节炎(OA)是一种年龄相关性退行性疾病，主要表现为关节软骨退行性变。许多炎症介质在OA患者中上调。丝裂原活化蛋白激酶(MAPK)和核因子-κB (NF-κB)通路在炎症反应的调控中发挥作用。自噬似乎表现出一种保护机制，并减轻大鼠OA的症状。SPRED2的失调与多种涉及炎症反应的疾病有关。然而，SPRED2在OA发展中的作用仍有待研究。目前的研究表明，SPRED2通过调节p38 MAPK信号通路促进IL-1β诱导的骨关节炎软骨细胞的自噬和减轻炎症反应。在OA患者膝关节软骨组织和il -1β诱导的软骨细胞中，SPRED2表达下调。SPRED2增强软骨细胞增殖，阻止IL-1β诱导的细胞凋亡。SPRED2抑制il -1β诱导的软骨细胞自噬和软骨细胞炎症反应。SPRED2抑制p38 MAPK信号通路的激活，改善OA软骨损伤。由此可见，SPRED2在体内通过调控p38 MAPK信号通路促进自噬，抑制炎症反应。

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来源期刊

Tissue & cell 医学-解剖学与形态学

CiteScore

3.90

自引率

0.00%

发文量

234

期刊介绍： Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.