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MicroRNA-1185 Induces Endothelial Cell Apoptosis by Targeting UVRAG and KRIT1

Haoyuan Deng1, Xia Chu1, Zhenfeng Song1

  • 1Department of Nutrition and Food Hygiene, Public Health College, Harbin Medical University, Harbin, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|April 26, 2017
PubMed
Abstract

Insights

MicroRNA-1185 promotes endothelial cell apoptosis, a key factor in atherosclerosis development. This finding suggests microRNA-1185 as a potential therapeutic target for preventing and treating this cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Genetics

Background:

  • Atherosclerosis is a leading cause of global mortality and morbidity.
  • Endothelial cell injury and apoptosis are critical in atherosclerosis development.
  • The role of apoptosis-related microRNAs in endothelial cells during atherogenesis requires further investigation.

Purpose of the Study:

  • To investigate the functional role of microRNA-1185 (miR-1185) in endothelial cell apoptosis.
  • To identify the molecular targets of miR-1185 involved in atherogenesis.

Main Methods:

  • Transfection of endothelial cells with miR-1185 and its inhibitor.
  • Bioinformatics analysis and luciferase reporter assays to identify miR-1185 targets.
  • Small-interfering RNA to assess the impact of miR-1185 targets on endothelial apoptosis.

Main Results:

  • miR-1185 significantly induced apoptosis in endothelial cells, but not in vascular smooth muscle cells or macrophages.
  • Ultraviolet irradiation resistance-associated gene (UVRAG) and krev1 interaction trapped gene 1 (KRIT1) were identified as direct targets of miR-1185.
  • UVRAG and KRIT1 mediated the pro-apoptotic effects of miR-1185 in endothelial cells.

Conclusions:

  • miR-1185 plays a significant role in promoting endothelial cell apoptosis.
  • miR-1185 targeting of UVRAG and KRIT1 contributes to its pro-apoptotic function.
  • miR-1185 represents a potential therapeutic target for atherosclerosis prevention and treatment.
Keywords:
ApoptosisEndotheliumKRIT1MiR-1185UVRAG

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