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BioMed Research International
Volume 2017 (2017), Article ID 6147294, 8 pages
https://doi.org/10.1155/2017/6147294
Research Article

Quercetin Inhibits Pulmonary Arterial Endothelial Cell Transdifferentiation Possibly by Akt and Erk1/2 Pathways

1Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China
2Laboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang 524001, China
3Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China
4Department of Cardiovascular Medicine, The People’s Hospital of Gaozhou, Maoming 525200, China
5Outpatient Operating Room, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China
6Tibetan Collaborative Innovation Center of Agricultural and Animal Husbandry Resources, Tibet Agricultural and Animal Husbandry College, Nyingchi 860000, China
7Laboratory of Vascular Surgery, Guangdong Medical University, Zhanjiang 524001, China
8Department of Pharmacology & Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH 45435, USA

Correspondence should be addressed to Can Chen and Wei Lei

Received 10 November 2016; Revised 18 February 2017; Accepted 23 February 2017; Published 27 March 2017

Academic Editor: Fabrizio Montecucco

Copyright © 2017 Shian Huang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This study aimed to investigate the effects and mechanisms of quercetin on pulmonary arterial endothelial cell (PAEC) transdifferentiation into smooth muscle-like cells. TGF-β1-induced PAEC transdifferentiation models were applied to evaluate the pharmacological actions of quercetin. PAEC proliferation was detected with CCK8 method and BurdU immunocytochemistry. Meanwhile, the identification and transdifferentiation of PAECs were determined by FVIII immunofluorescence staining and α-SMA protein expression. The related mechanism was elucidated based on the levels of Akt and Erk1/2 signal pathways. As a result, quercetin effectively inhibited the TGF-β1-induced proliferation and transdifferentiation of the PAECs and activation of Akt/Erk1/2 cascade in the cells. In conclusion, quercetin is demonstrated to be effective for pulmonary arterial hypertension (PAH) probably by inhibiting endothelial transdifferentiation possibly via modulating Akt and Erk1/2 expressions.