Open AccessDifferentially Expressed MicroRNAs Associated with Vein Graft Restenosis in Rats
Author(s) -
Shuwei Wan,
Hui Cao,
Yuchong Zhao,
Yaming Guo,
Chuang Li,
Nan Li,
Can Cao,
Zhaohui Hua,
Zhen Li
Publication year - 2020
Publication title -
cardiovascular innovations and applications
Language(s) - English
Resource type - Journals
eISSN - 2009-8782
pISSN - 2009-8618
DOI - 10.15212/cvia.2019.0584
Subject(s) - restenosis , intimal hyperplasia , microrna , neointima , medicine , neointimal hyperplasia , hyperplasia , transplantation , h&e stain , wnt signaling pathway , pathology , immunohistochemistry , biology , signal transduction , gene , microbiology and biotechnology , stent , smooth muscle , biochemistry
Objective: Intimal hyperplasia is the main cause of restenosis of vein grafts after venous transplantation. MicroRNAs are considered to play a role in vein graft restenosis; however, the expression profile of microRNAs in neointima has not been reported in detail. We wanted to investigate the differentially expressed microRNAs in the restenosis of vein grafts in rats. Methods: We established a rat model for vein transplantation to explore the pathogenic roles of microRNAs during intimal hyperplasia. Hematoxylin and eosin staining was used to confirm intimal hyperplasia in the vein grafts. Changes in microRNA expression in the vein grafts were detected 3 and 14 days after surgery by sequencing, reverse transcription‐quantitative polymerase chain reaction, and bioinformatics analyses for functional annotation. Results: We detected 711 newly predicted microRNAs among all the comparisons. Among these comparisons, 437 differentially expressed microRNAs were detected in the postoperative day 3 group versus the control group, 265 were detected in the postoperative day 14 group versus the control group, and 158 were detected in the postoperative day 14 group versus the postoperative day 3 group. Pathway analysis revealed significant enrichment of target genes that mediate Wnt, mitogen-activated protein kinase, vascular smooth muscle contraction, and regulation of actin cytoskeleton signaling. Conclusion: Our results provide insight into the pathogenesis of restenosis and will help develop novel targets in the prevention and treatment of vein graft restenosis.