MiR-423-5p promotes angiogenesis by targeting LHX6 in oxygen–glucose deprivation and reperfusion (OGD/R) induced Human Umbilical Vein Endothelial Cells (HUVEC)

Abstract

Abstract Background The prognosis of ischemic stroke is poor, moreover, ischemia-reperfusion (I/R) injury following revascularization therapy can give rise to more severe outcomes. Therefore, finding other effective and new methods for treating ischemic stroke is necessary. According to studies some microRNAs are involved in the process of angiogenesis which plays an increasingly vital role in I/R injury. In the present study, We selected miR-423-5p as our research object because of our previous clinical results. Methods To contrust the I/R injury model in vitro, we used oxygen–glucose deprivation and reperfusion (OGD/R) induced Human Umbilical Vein Endothelial Cells (HUVEC) as our study subjects. The level of miR-423-5p expression was detected by reverse transcription quantitative polymerase chain reaction(RT-qPCR). Transwell assay, scratch assay and tube formation assay were used to evaluate the proangiogenic activity with miR-423-5p mimic or inhibitor in vitro. We adopted western blot and RT-qPCR to test the expression of LIM homeobox 6(LHX6), and a luciferase reporter assay was carried out to confirm whether LHX6 is a direct target of miR-423-5p. Results We found miR-423-5p was significantly down-regulated in OGD/R induced HUVEC. The overexpression of miR-423-5p stimulated HUVEC proliferation and migration, instead, miR-423-5p inhibitor played the opposite role. In further research, we identified LHX6 as a downstream gene of miR-423-5p by the luciferase reporter assay. Western blot and RTqPCR analysis confirmed that LHX6 expression was negatively related to the expression of miR-423-5p. Conclusions In summary, this study suggests that miR-423-5p mediated the proangiogenic activity of HUVEC by relying on LHX6. It could be an underlying therapeutic target for I/R injury that warrants further studies.