Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 532, Issue 3, Pages 400-405Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.08.064
Keywords
Pulmonary arterial hypertension; Vascular remodeling; Pulmonary artery smooth muscle cells; Mesenchymal stem cells; TNF alpha
Categories
Funding
- Major projects of Natural Science Research in Colleges and Universities of Anhui Province [KJ2018ZD023]
- Anhui Province Education Key Projects [KJ2019A0303]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars of Ministry of Education of China [46th-Department of International Cooperation and Communication of the Ministry of Education(2013)693]
- Excellent Young Talent Project in Colleges and Universities of Anhui Province [gxyq2018039]
Ask authors/readers for more resources
Hypoxia could cause vascular smooth muscle hypertrophy, leading to high pulmonary circulation resistance, pulmonary artery (PA) pressure, even pulmonary arterial hypertension (PAH). Recent studies have demonstrated the ability of mesenchymal stem cell (MSC) to ameliorate PAH but the mechanism was controversial. In this study, we revealed that the growth rate of pulmonary artery smooth muscle cells (PASMCs) treated with hypoxia was significantly increased than normal and showed lower expression of potassium channels. However, cells co-cultured with MSC showed decreased proliferation capability and down-regulated expression of ion channel of PAMSCs. The protein array data showed that the changes of PAMSCs was substantially associated with a high level of tumor necrosis factor alpha (TNFa) secretion from MSC. We further demonstrated that TNF alpha rescued the cell behavior of PAMSCs through activating the expression of P53 and NF-kB and inducing cell cycle arrest by P21/CDK2/CDK4 downregulation. These findings suggested that MSCs could attenuate abnormal function of PAMSCs by TNF alpha secretion, which was more or less associated with the beneficial effects of MSC on improving PAH. (C) 2020 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available