Cellular Physiology and Biochemistry (May 2015)

MicroRNA-130a Targets MAP3K12 to Modulate Diabetic Endothelial Progenitor Cell Function

  • Meng Ye,
  • Dan Li,
  • Jian Yang,
  • Jing Xie,
  • Fei Yu,
  • Yushui Ma,
  • Xuchao Zhu,
  • Jinwei Zhao,
  • Zhongwei Lv

DOI
https://doi.org/10.1159/000430132
Journal volume & issue
Vol. 36, no. 2
pp. 712 – 726

Abstract

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Aims: The aim of the present study was to explore the influence of microRNA (miR)-130a dysregulation on the JNK signal pathway through its target MAP3K12 in diabetic endothelial progenitor cells (EPCs). Methods: The expression of miR-130a was compared between diabetic and normal EPCs. Computational target prediction was performed to identify MAP3K12 as a functionally relevant target of miR-130a in EPCs. The role of miR-130a was investigated regarding its anti-apoptotic effects and its role on the regulation of EPC function was evaluated through the negative regulation of the JNK signal pathway Results: MiR-130a expression was significantly downregulated in diabetic EPCs, and cell proliferation was reduced in EPCs under high glucose condition. miR-130a inhibited the JNK pathway by targeting MAP3K12, contributing to its anti-apoptotic effect and the maintenance of EPC function. In diabetic EPCs, high glucose affects the expression of miR-130a, inducing sustained JNK activation and promoting EPC apoptosis and dysfunction. Conclusions: Downregulation of miR-130a may underlie endothelial dysfunction in diabetes through the activation of JNK signal pathway.

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