Altered extracellular matrix remodeling accompanies decreased lncRNA HOTAIR expression in Takayasu arteritis

大动脉炎中细胞外基质重塑改变伴随lncRNA HOTAIR表达降低

阅读:2

Abstract

OBJECTIVES: Takayasu arteritis (TAK) is a large-vessel vasculitis characterized by chronic vascular inflammation and extracellular matrix (ECM) remodeling. Long non-coding RNAs (lncRNAs) have emerged as epigenetic regulators of inflammatory and structural vascular processes. This study aimed to evaluate whether lncRNA HOTAIR (HOX transcript antisense RNA) expression in peripheral blood mononuclear cells (PBMCs) is associated with circulating mediators involved in ECM turnover in patients with TAK. METHODS: Fifty-three patients with angiographically confirmed TAK and 53 age- and sex-matched healthy controls were recruited. HOTAIR expression in PBMCs was quantified by reverse transcription-quantitative polymerase chain reaction. Serum concentrations of matrix metalloproteinase-1 (MMP-1), MMP-2, MMP-3, MMP-9, MMP-13, tissue inhibitor of metalloproteinases-1 (TIMP-1), TIMP-3, extracellular matrix metalloproteinase inducer (EMMPRIN)/CD147, and galectin-3 were measured using enzyme-linked immunosorbent assays. RESULTS: Compared with controls, TAK patients exhibited significantly higher serum levels of MMP-2 (2245 [1929–2646] vs. 1868 [1576–2355] pg/mL; p=0.036), TIMP-1 (2811 [2644–3216] vs. 2588 [2309–2770] pg/mL; p=0.006), and EMMPRIN/CD147 (1494 [1264–2115] vs. 1310 [1132–1655] pg/mL; p=0.035), along with a reduced MMP-9/TIMP-1 ratio (0.88 [0.61–1.28] vs. 1.18 [0.91–1.41]; p=0.006). HOTAIR expression was markedly downregulated in TAK patients (8.05 [2.52–24.54] vs. 36.09 [30.08–43.85] arbitrary units; p=0.006) and was not associated with disease activity. Notably, HOTAIR expression inversely correlated with circulating MMP-2 (Spearman’s rho -0.276) and EMMPRIN/CD147 (Spearman’s rho -0.280) levels. CONCLUSION: TAK displays a circulating proteolytic profile consistent with enhanced ECM turnover and vascular remodeling. The marked downregulation of HOTAIR supports the involvement of epigenetic mechanisms in TAK and suggests a potential association between reduced HOTAIR expression and MMP-mediated vascular injury.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。