miR-146a and miR-146b regulate the expression of ICAM-1 in giant cell arteritis

巨细胞动脉炎 转染 小RNA 生物 细胞因子 离体 活力测定 基因表达 细胞培养 基因表达调控 分子生物学 体内 癌症研究 医学 免疫学 基因 病理 血管炎 疾病 遗传学
作者
Martina Bonacini,Alessandro Rossi,Ilaria Ferrigno,Francesco Muratore,Luigi Boiardi,Alberto Cavazza,Alessandra Bisagni,Luca Cimino,Luca De Simone,Angelo Ghidini,Giuseppe Malchiodi,Marc Corbera‐Bellalta,María C. Cid,Alessandro Zerbini,Carlo Salvarani,Stefania Croci
出处
期刊:Journal of Autoimmunity [Elsevier]
卷期号:144: 103186-103186 被引量:1
标识
DOI:10.1016/j.jaut.2024.103186
摘要

Giant cell arteritis (GCA) is an inflammatory disease of large/medium-sized arteries. MiRNAs are small, non-coding RNAs that inhibit gene expression at post-transcriptional level. Several miRNAs have been shown to be dysregulated in temporal artery biopsies (TABs) from GCA patients, but their role is unknown. The aims of the present work were: to gain insight into the link between inflammation and miRNA up-regulation in GCA; to identify the role of miR-146a and miR-146b. Primary cultures from TABs were treated with IL-1β, IL-6, soluble IL-6R (sIL6R), IL-17, IL-22, IFNγ, LPS and PolyIC. Correlations between cytokine mRNA and miRNA levels were determined in inflamed TABs. Primary cultures from TABs, human aortic endothelial and smooth muscle cells and ex-vivo TAB sections were transfected with synthetic miR-146a and miR-146b to mimic miRNA activities. Cell viability, target gene expression, cytokine levels in culture supernatants were assayed. Treatment of primary cultures from TABs with IL-1β and IL-17 increased miR-146a expression while IL-1β, IL-6+sIL6R and IFNγ increased miR-146b expression. IFNγ and IL-1β mRNA levels correlated with miR-146a/b levels. Following transfection, cell viability decreased only in primary cultures from TABs. Moreover, transfection of miR-146a/b mimics increased ICAM-1 gene expression and production of the soluble form of ICAM-1 by primary cultures from TABs and by ex-vivo TABs. ICAM-1 expression was higher in inflamed than normal TABs and ICAM-1 levels correlated with miR-146a/b levels. Expression of miR-146a and miR-146b in GCA appeared to be driven by inflammatory cytokines (e.g. IL-1β, IFNγ). miR-146a and miR-146b seem responsible for the increase of soluble ICAM-1.
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