Abstract

Endothelial progenitor cells (EPCs) play an important role in tissue repair after ischemic heart disease. In particular, the recovery of endothelial function is reliant on the ability and rate of EPCs differentiate into mature endothelial cells. The present study evaluated the effect of microRNA 107 (miR-107) on the mechanism of EPCs differentiation. EPCs were isolated from rats' bone marrow and miR-107 expression of EPCs in hypoxic and normoxic conditions were measured by real-time qualitative PCR. CD31 was analyzed by flow cytometry and eNOS was examined by real-time qualitative PCR and western blotting and these were used as markers of EPC differentiation. In order to reveal the mechanism, we used miR107 inhibitor and lentiviral vector expressing a short hairpin RNA (shRNA) that targets miR-107 and hypoxia-inducible factor-1 β (HIF-1β) to alter miR107 and HIF-1β expression. MiR-107 expression were increased in EPCs under hypoxic conditions. Up-regulation of miR-107 partly suppressed the EPCs differentiation induced in hypoxia, while down-regulation of miR-107 promoted EPC differentiation. HIF-1β was the target. This study indicated that miR-107 was up-regulated in hypoxia to prevent EPCs differentiation via its target HIF-1β. The physiological mechanisms of miR-107 must be evaluated if it is to be used as a potential anti-ischemia therapeutic regime.

Highlights

  • Ischemic heart disease is one of the most prominent health problems throughout the world and carries with it a high mortality rate

  • We found that hypoxia-inducible factor-1a (HIF-1a) knockdown via adenoviral small interfering RNA transfer inhibited endothelial progenitor cells (EPCs) differentiation [9]

  • Previous studies have shown that overexpression of HIF-1a promotes the differentiation of EPCs ex vivo [12], while HIF-1a knockdown via adenoviral small interfering RNA (siRNA) inhibits EPCs differentiation

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Summary

Introduction

Ischemic heart disease is one of the most prominent health problems throughout the world and carries with it a high mortality rate. Circulating endothelial progenitor cells (EPCs) are mobilized from the bone marrow in response to tissue ischemia [1]. At sites of vessel injury, EPCs can differentiate into mature endothelial cells and are known to play critical role in tissue repair and endothelial function recovery [2,3]. HIF-1a heterodimerizes with hypoxia-inducible factor-1 b (HIF-1b), which is another subunit of HIF-1. We found that HIF-1a knockdown via adenoviral small interfering RNA (siRNA) transfer inhibited EPC differentiation [9]. It is still unknown how HIF-1b, which heterodimerized with HIF-1a, acts during EPC differentiation in hypoxic conditions

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