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

Author:

Huang Shian123,Zhu Xiulong4,Huang Wenjun5,He Yuan4,Pang Lingpin1,Lan Xiaozhong6,Shui Xiaorong237,Chen Yanfang38ORCID,Chen Can123ORCID,Lei Wei123ORCID

Affiliation:

1. Cardiovascular Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China

2. Laboratory of Cardiovascular Diseases, Guangdong Medical University, Zhanjiang 524001, China

3. Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China

4. Department of Cardiovascular Medicine, The People’s Hospital of Gaozhou, Maoming 525200, China

5. Outpatient Operating Room, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China

6. Tibetan Collaborative Innovation Center of Agricultural and Animal Husbandry Resources, Tibet Agricultural and Animal Husbandry College, Nyingchi 860000, China

7. Laboratory of Vascular Surgery, Guangdong Medical University, Zhanjiang 524001, China

8. Department of Pharmacology & Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH 45435, USA

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 andα-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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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