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MicroRNA-216b actively modulates diabetic angiopathy through inverse regulation on FZD5

Yuxiang Dai1, Hao Lu1, Shen Wang2

  • 1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Gene
|February 26, 2018
PubMed
Abstract

Insights

MicroRNA-216b is overexpressed in diabetic heart cells, and reducing it boosts blood vessel growth. This suggests a new target for treating diabetic blood vessel disease by regulating FZD5.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Endothelial Cell Function

Background:

  • Diabetic angiopathy involves abnormal blood vessel growth.
  • MicroRNAs play a role in regulating cellular processes.
  • Myocardial microvascular endothelial cells (MMECs) are crucial for heart blood supply.

Purpose of the Study:

  • To investigate the role of microRNA-216b in diabetic angiogenesis.
  • To explore the relationship between microRNA-216b and its target gene FZD5 in MMECs.

Main Methods:

  • Cultured MMECs from Wistar and diabetic Goto-Kakizaki rats.
  • Quantified microRNA-216b levels using qRT-PCR.
  • Assessed angiogenic functions (invasion, proliferation).
  • Validated FZD5 as a target using luciferase assays, qRT-PCR, and Western blot.

Main Results:

  • MicroRNA-216b was overexpressed in diabetic MMECs.
  • Downregulating microRNA-216b enhanced MMEC invasion and proliferation.
  • FZD5 expression was inversely correlated with microRNA-216b levels.
  • FZD5 downregulation inhibited angiogenesis in diabetic MMECs.

Conclusions:

  • MicroRNA-216b is upregulated in diabetic MMECs.
  • Downregulation of microRNA-216b promotes angiogenesis in diabetic conditions.
  • This effect is mediated through the inverse regulation of FZD5.
Keywords:
AngiopathyFZD5Microvascular, endothelialType-II diabetesmiR-216b

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