Hypoxia-activated platelets stimulate proliferation and migration of pulmonary arterial smooth muscle cells by phosphatidylserine/LOX-1 signaling-impelled intercellular communication.


Journal

Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683

Informations de publication

Date de publication:
11 2021
Historique:
received: 25 06 2021
revised: 23 08 2021
accepted: 09 09 2021
pubmed: 15 9 2021
medline: 1 4 2022
entrez: 14 9 2021
Statut: ppublish

Résumé

Continuous recruitment and inappropriate activation of platelets in pulmonary arteries contribute to pulmonary vascular remodeling in pulmonary hypertension (PH). Our previous study has demonstrated that lectin like oxidized low-density lipoprotein receptor-1 (LOX-1) regulates the proliferation of pulmonary arterial smooth muscle cells (PASMCs). Phosphatidylserine exposed on the surface of activated platelets is a ligand for LOX-1. However, whether hypoxia-activated platelets stimulate the proliferation and migration of PASMCs by phosphatidylserine/LOX-1 signaling-impelled intercellular communication remains unclear. The present study found that rats treated with hypoxia (10% O

Identifiants

pubmed: 34520855
pii: S0898-6568(21)00238-2
doi: 10.1016/j.cellsig.2021.110149
pii:
doi:

Substances chimiques

Phosphatidylserines 0
Scavenger Receptors, Class E 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

110149

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Auteurs

Xiaoyue Ge (X)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China.

Weifang Zhang (W)

Department of Pharmacy, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.

Tiantian Zhu (T)

Teaching and Research Office of Clinical Pharmacology, College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, Henan, China.

Ning Huang (N)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China.

Maozhong Yao (M)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China.

Hong Liu (H)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China.

Di Wang (D)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China.

Guangxuan Zhu (G)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China.

Zheng Zhang (Z)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China; Human Provincial Key Laboratory of Cardiovascular Research, Central South University, Changsha 410078, Hunan, China.

Changping Hu (C)

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, Hunan, China; Human Provincial Key Laboratory of Cardiovascular Research, Central South University, Changsha 410078, Hunan, China. Electronic address: huchangping@csu.edu.cn.

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Classifications MeSH