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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Research Article

Qiliqiangxin Prescription Promotes Angiogenesis of Hypoxic Primary Rat Cardiac Microvascular Endothelial Cells via Regulating miR-21 Signaling

Author(s):Yanyan Wang*,Jingjing Zhang, Mingqiang Fu,Jingfeng Wang,Xiaotong Cui,Yu Song,Xueting Han, Yuan Liu,Jingmin Zhou* andJunbo Ge*

Volume 27, Issue 26, 2021

Published on: 05 October, 2020

Page: [2966 - 2974]Pages: 9

DOI:10.2174/1381612826666201005152709

Price: $65

TIMBC 2025
Abstract

Background and Objective: Angiogenesis is the most important repair process of tissues subjectedto 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 SDrats by the method of planting myocardium tissues. The purity was identified by CD31 immunofluorescencestaining. CMECs were then cultured under 1% O2 hypoxia or normoxia condition for 24h in the presence orabsence of QL pretreatment (QL, 0.5mg/ml, 24h). The mimics and inhibitors of miR-21 were transfected intoCMECs. miR-21, HIF-1α, and VEGF expressions of CMECs were then detected by qRT-PCR and/or Westernblot. 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 expressionof miR-21 and impaired CMECs proliferation, migration, and tube formation functions. Compared withthe 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 knockdownof miR-21. Conversely, treatment with miR-21 mimics further enhanced QL induced changes in hypoxicCMECs.

Conclusion: Results indicate that the pro-angiogenesis effects of QL on hypoxic CMECs are mediated by activatingmiR-21 and its downstream HIF-1α/VEGF pathway possibly.

Keywords:Qiliqiangxin prescription, cardiac microvascular endothelial cells, hypoxia, miR-21, angiogenesis, proliferation.


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Current Pharmaceutical Design

Title:Qiliqiangxin Prescription Promotes Angiogenesis of Hypoxic Primary Rat Cardiac Microvascular Endothelial Cells via Regulating miR-21 Signaling

Volume: 27Issue: 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 subjectedto 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 SDrats by the method of planting myocardium tissues. The purity was identified by CD31 immunofluorescencestaining. CMECs were then cultured under 1% O2 hypoxia or normoxia condition for 24h in the presence orabsence of QL pretreatment (QL, 0.5mg/ml, 24h). The mimics and inhibitors of miR-21 were transfected intoCMECs. miR-21, HIF-1α, and VEGF expressions of CMECs were then detected by qRT-PCR and/or Westernblot. 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 expressionof miR-21 and impaired CMECs proliferation, migration, and tube formation functions. Compared withthe 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 knockdownof miR-21. Conversely, treatment with miR-21 mimics further enhanced QL induced changes in hypoxicCMECs.

                Conclusion: Results indicate that the pro-angiogenesis effects of QL on hypoxic CMECs are mediated by activatingmiR-21 and its downstream HIF-1α/VEGF pathway possibly.

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                About this article

                Cite this article as:

                Wang Yanyan *, Zhang Jingjing , Fu Mingqiang , Wang Jingfeng , Cui Xiaotong , Song Yu , Han Xueting , Liu Yuan , Zhou Jingmin *, Ge Junbo *,Qiliqiangxin Prescription Promotes Angiogenesis of Hypoxic Primary Rat Cardiac Microvascular Endothelial Cells via Regulating miR-21 Signaling, Current Pharmaceutical Design 2021; 27 (26) .https://dx.doi.org/10.2174/1381612826666201005152709

                DOI
                https://dx.doi.org/10.2174/1381612826666201005152709
                Print ISSN
                1381-6128
                Publisher Name
                Bentham Science Publisher
                Online ISSN
                1873-4286

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