MiR-497-5p Ameliorates Deep Venous Thrombosis by Facilitating Endothelial Progenitor Cell Migration and Angiogenesis by Regulating LITAF.

IF 2.1 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochemical Genetics Pub Date : 2024-10-21 DOI:10.1007/s10528-024-10927-x

Shuguo Xu, Zhihong Yang, Longbiao Li, Yuansheng Cui, Zhen Chen

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Abstract

Deep vein thrombosis (DVT) is a clinical manifestation of venous thromboembolism and a major global burden of cardiovascular disease. In recent years, the crucial role of microRNAs (miRNAs) in cardiovascular disease has been confirmed. Here, we aimed to investigate the specific effect of miR-497-5p on DVT. The endothelial progenitor cells (EPCs) were obtained from the bone marrow of newborn rats and transfected with miR-497-5p mimics or/and pcDNA3.1/lipopolysaccharide-induced TNF factor (LITAF). The proliferation and migration abilities of EPCs were detected using CCK-8 assay and transwell assay, respectively. Angiogenesis was evaluated using tube formation assay. The interaction of miR-497-5p and LITAF was confirmed by luciferase reporter experiment. DVT rat model in vivo was established by inferior vena cava (IVC) ligation in Sprague-Dawley rats. Histological analysis of IVC tissue was conducted by hematoxylin-eosin staining. We found that enhancing miR-497-5p expression facilitated the abilities of proliferation and migration of EPCs. Additionally, overexpression of miR-497-5p increased the capacity of EPCs to form capillary tubes on Matrigel. LITAF was found to be targeted by miR-497-5p and negatively regulated by miR-497-5p. Overexpression of LITAF counteracted the miR-497-5p overexpression's effect on the proliferation, migration, and angiogenesis abilities of EPCs. Moreover, the injection of agomir-miR-497-5p alleviated thrombus formation, reduced thrombus weight, and reduced the serum level of D-dimer in DVT rat model by reducing LITAF expression. This study suggests that miR-497-5p alleviates DVT by facilitating EPCs proliferation, migration, and angiogenesis by targeting LITAF.

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MiR-497-5p 通过调控 LITAF 促进内皮祖细胞迁移和血管生成，从而改善深静脉血栓形成。

深静脉血栓（DVT）是静脉血栓栓塞症的一种临床表现，也是全球心血管疾病的主要负担。近年来，微小RNA（miRNA）在心血管疾病中的关键作用已被证实。在此，我们旨在研究 miR-497-5p 对深静脉血栓的特殊作用。我们从新生大鼠骨髓中获得了内皮祖细胞（EPCs），并用 miR-497-5p mimics 或/和 pcDNA3.1/lipopolysaccharide-induced TNF factor（LITAF）转染了这些细胞。分别使用 CCK-8 试验和 transwell 试验检测 EPCs 的增殖和迁移能力。利用血管形成试验评估了血管生成情况。荧光素酶报告实验证实了 miR-497-5p 与 LITAF 的相互作用。通过在 Sprague-Dawley 大鼠体内结扎下腔静脉（IVC）建立了深静脉血栓大鼠模型。通过苏木精-伊红染色对 IVC 组织进行组织学分析。我们发现，提高 miR-497-5p 的表达可促进 EPCs 的增殖和迁移能力。此外，miR-497-5p的过表达还提高了EPCs在Matrigel上形成毛细管的能力。研究发现，LITAF是miR-497-5p的靶标，并受miR-497-5p的负调控。LITAF的过表达抵消了miR-497-5p过表达对EPCs增殖、迁移和血管生成能力的影响。此外，注射 agomir-miR-497-5p 还能通过减少 LITAF 的表达，缓解深静脉血栓大鼠模型中血栓的形成、减轻血栓重量并降低血清中 D-二聚体的水平。这项研究表明，miR-497-5p 可通过靶向 LITAF 促进 EPCs 增殖、迁移和血管生成，从而缓解深静脉血栓。

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来源期刊

Biochemical Genetics 生物-生化与分子生物学

CiteScore

3.90

自引率

0.00%

发文量

133

审稿时长

4.8 months

期刊介绍： Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses. Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication. Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses. Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods. Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.