microRNA-126 inhibits tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway

It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs w...

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Veröffentlicht in:Biomedicine & pharmacotherapy 2019-08, Vol.116, p.109007-109007, Article 109007
Hauptverfasser: Li, Qiang, Cheng, Kai, Wang, Ai-Yue, Xu, Qiong-Guang, Fu, Zhou-Feng, He, Shao-Yu, Xu, Peng-Xiang
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Sprache:eng
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Zusammenfassung:It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs were cultured and transfected with microRNA-126 mimics and miR-126 inhibitor. Cell counting kit-8 (CCK-8) and cell cycle assay were conducted for evaluating NSCs viability. Transwell assay was conducted to observe invasive ability of HUVECs. Quantitative real-time PCR (qRT-PCR) assay was used to examine epidermal growth factor like domain 7 (EGFL7) and miR-126 mRNA both in vitro and animal models. Tube forming capability was evaluated in HUVECs. Dual luciferase assay was performed to evaluate interaction between miR-126 and EGFL7 gene. Western blot assay was used to determine phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling molecules and EGFL7. The results indicated that miR-126 significantly decreased cell viability, inhibited invasive ability and modulated cell cycle of NSCs compared to miR-NC group (p 
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2019.109007