Open AccessKnockdown of Microrna-1260 Promotes Up-Regulation of Both Collagen Type 1 Alpha 1 and Monocyte Chemoattractant Protein-1 in Vascular Smooth Muscle Cells from Human Abdominal Aortic Tissues
Author(s) -
Crystal Yin Tung Chan,
B.L.Y. Cheuk,
Stephen W.K. Cheng
Publication year - 2020
Publication title -
annals of vascular medicine and research
Language(s) - English
Resource type - Journals
ISSN - 2378-9344
DOI - 10.47739/vascularmedicine.1103
Subject(s) - gene knockdown , vascular smooth muscle , matrix metalloproteinase , mmp1 , elastin , microrna , apoptosis , inflammation , microbiology and biotechnology , downregulation and upregulation , tissue inhibitor of metalloproteinase , chemistry , cancer research , biology , medicine , endocrinology , immunology , pathology , gene expression , gene , biochemistry , smooth muscle
Objectives: MicroRNA (miR)-1260 was identified to be down-regulated in vascular smooth muscle cells (VSMCs) from human abdominal aortic aneurysm (AAA) tissues in our previous microarray profiling assay. MiR-1260 was predicted to target and down-regulate collagen type 1 alpha 1 (COL1A1), which is closely related to AAA formation, from a bioinformatics analysis. However, the role of miR-1260 in VSMCs for AAA formation still remains uncertain. This study aims to investigate the role of miR-1260 in human VSMCs. Methods: Stable overexpression and knockdown of miR-1260 using lentivirus were performed in VSMCs cultured from human abdominal aortic tissues. Expression of COL1A1 protein was investigated, followed by investigating the expressions of several key components involved in AAA pathogenic features: monocyte chemoattractant protein-1 (MCP-1) for inflammation; matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of matrix metalloproteinase (TIMP)- 1 and TIMP-2 for elastin fragmentation. Apoptosis of VSMCs was also examined. Results: Both COL1A1 and MCP-1 were significantly down-regulated upon miR-1260 overexpression, whereas they were significantly up-regulated upon miR-1260 knockdown. Neither protein expressions of MMP-2, MMP-9, TIMP-1 and TIMP-2 nor apoptosis were significantly different between miR-1260 overexpression/knockdown and corresponding controls. Conclusions: Our findings suggested suppression of miR-1260, which was previously found associated with AAA VSMCs, may promote up-regulation of COL1A1 and MCP-1 in human VSMCs, possibly promoting compensatory collagen synthesis and inflammation for AAA formation.