Decreased expression of circ_0020397 in intracranial aneurysms may be contributing to decreased vascular smooth muscle cell proliferation via increased expression of miR-138 and subsequent decreased KDR expression

Cell Adh Migr. 2019 Dec;13(1):220-228. doi: 10.1080/19336918.2019.1619432.

Abstract

Dysfunction of vascular smooth muscle cells (VSMCs) mediates intracranial aneurysm (IA). KDR is reported to alleviate IA progression via promoting VSMC proliferation, while the upstream regulators are still unclear. Arterial wall tissues at the aneurysm site from 12 patients were obtained. The real-time PCR result indicated that circRNA_0020397 was down-regulated, but miR-138 was up-regulated in artery wall tissues and cells of IA. Overexpressed circRNA_0020397 promoted proliferation of human umbilical artery SMCs. MiR-138 negatively regulated KDR via binding with 3'UTR of KDR mRNA. The expression of circRNA_0020397 was negatively correlated with miR-138. In conclusion, our findings demonstrated that decreased expression of circRNA_0020397 in IA may contribute to the decreased VSMC proliferation via increasing miR-138 expression and subsequently decreasing KDR expression.

Keywords: Intracranial aneurysm; KDR; cell proliferation; circ_0020397; miR-138.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Cell Movement
  • Cell Proliferation*
  • Cells, Cultured
  • Gene Expression Regulation
  • Humans
  • Intracranial Aneurysm / genetics
  • Intracranial Aneurysm / metabolism
  • Intracranial Aneurysm / pathology*
  • Meningeal Arteries / cytology*
  • Meningeal Arteries / metabolism
  • MicroRNAs / genetics*
  • Muscle, Smooth, Vascular / cytology*
  • Muscle, Smooth, Vascular / metabolism
  • RNA, Circular / genetics*
  • Signal Transduction
  • Vascular Endothelial Growth Factor Receptor-2 / genetics
  • Vascular Endothelial Growth Factor Receptor-2 / metabolism*

Substances

  • MIRN138 microRNA, human
  • MicroRNAs
  • RNA, Circular
  • KDR protein, human
  • Vascular Endothelial Growth Factor Receptor-2

Grants and funding

The present study was supported by the Key Science and Technology Project of Henan Science and Technology Department (172102310100).