CircSEC24A在IL-1β诱导的骨关节炎中的调节作用和机制

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-09-27 DOI:10.1080/13813455.2024.2404975
Yuanrui Wang, Xiaochao Chen, Yongfeng Chen, Qiang Sun, Huayi Wang
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引用次数: 0

摘要

骨关节炎(OA)是一种以关节软骨退化和损伤为特征的慢性关节疾病。目前已发现越来越多的环状 RNA(circRNA)参与了 OA 的发病机制。据报道,Hsa_circ_0128006(又称 circSEC24)是一种在 OA 组织中上调的 circRNA,但其在 OA 中的生物学作用和潜在机制仍有待讨论。在 OA 软骨组织和 IL-1β 处理的 CHON-001 细胞中,circSEC24A 和 NAMPT 表达水平上调,miR-515-5p 表达水平降低。缺失circSEC24A会抑制IL-1β诱导的细胞活力,并促进CHON-001细胞的氧化应激、凋亡、细胞外基质(ECM)降解和炎症。从机理上讲,circSEC24A 是 miR-515-5p 影响 NAMPT 表达的分子海绵。circSEC24A敲除可部分通过miR-515-5p/NAMPT轴减轻IL-1β诱发的CHON-001细胞损伤,为circSEC24A在OA治疗中的潜在应用提供了新的见解。
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Regulatory effect and mechanism of CircSEC24A in IL-1β-induced osteoarthritis.

Osteoarthritis (OA) is a chronic joint disease characterized by articular cartilage degeneration and damage. Increasing circular RNAs (circRNAs) have been identified to participate in the pathogenesis of OA. Hsa_circ_0128006 (also known as circSEC24) was reported as an upregulated circRNA in OA tissues, but its biological role and underlying mechanism in OA are still to be discussed. circSEC24A and NAMPT expression levels were upregulated, and miR-515-5p was reduced in OA cartilage tissues and IL-1β-treated CHON-001 cells. The absence of circSEC24A overturned IL-1β-induced suppression of cell viability and promotion of oxidative stress, apoptosis, extracellular matrix (ECM) degradation, and inflammation in CHON-001 cells. Mechanistically, circSEC24A acted as a molecular sponge for miR-515-5p to affect NAMPT expression. CircSEC24A knockdown could attenuate IL-1β-triggered CHON-001 cell injury partly via the miR-515-5p/NAMPT axis, providing new insight into the underlying application of circSEC24A in OA treatment.

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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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