Title:Qiliqiangxin Prescription Promotes Angiogenesis of Hypoxic Primary Rat Cardiac Microvascular Endothelial Cells via Regulating miR-21 Signaling
Volume: 27
Issue: 26
Author(s): Yanyan Wang*, Jingjing Zhang, Mingqiang Fu, Jingfeng Wang, Xiaotong Cui, Yu Song, Xueting Han, Yuan Liu, Jingmin Zhou*Junbo Ge*
Affiliation:
- Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, 200032, Shanghai,China
- Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, 200032, Shanghai,China
- Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, 200032, Shanghai,China
Keywords:
Qiliqiangxin prescription, cardiac microvascular endothelial cells, hypoxia, miR-21, angiogenesis, proliferation.
Abstract:
Background and Objective: Angiogenesis is the most important repair process of tissues subjected
to ischemic injury. The present study aims to investigate whether the pro-angiogenic effect of Qiliqiangxin prescription
(QL) is mediated through miR-21 signaling.
Methods: Cardiac microvascular endothelial cells (CMECs) were isolated and cultured from 2-3 weeks old SD
rats by the method of planting myocardium tissues. The purity was identified by CD31 immunofluorescence
staining. CMECs were then cultured under 1% O2 hypoxia or normoxia condition for 24h in the presence or
absence of QL pretreatment (QL, 0.5mg/ml, 24h). The mimics and inhibitors of miR-21 were transfected into
CMECs. miR-21, HIF-1α, and VEGF expressions of CMECs were then detected by qRT-PCR and/or Western
blot. The proliferation, migration, and tube formation functions of CMECs were assessed using the BrdU assay,
wound healing test, and tube formation assay, respectively.
Results: The results showed that compared with the control group, hypoxia significantly upregulated the expression
of miR-21 and impaired CMECs proliferation, migration, and tube formation functions. Compared with
the hypoxia group, QL further upregulated miR-21, HIF-1α, and VEGF expressions, and improved cell proliferation,
migration, and tube formation of hypoxic CMECs. These effects of QL were abolished by a knockdown
of miR-21. Conversely, treatment with miR-21 mimics further enhanced QL induced changes in hypoxic
CMECs.
Conclusion: Results indicate that the pro-angiogenesis effects of QL on hypoxic CMECs are mediated by activating
miR-21 and its downstream HIF-1α/VEGF pathway possibly.
