Dihydroartemisinin inhibits endothelial cell migration via the TGF-β1/ALK5/SMAD2 signaling pathway.

TGF-β1/ALK5/SMAD2 pathway angiogenesis dihydroartemisinin endothelial cell migration

Journal

Experimental and therapeutic medicine
ISSN: 1792-0981
Titre abrégé: Exp Ther Med
Pays: Greece
ID NLM: 101531947

Informations de publication

Date de publication:
Jul 2021
Historique:
received: 01 09 2020
accepted: 12 03 2021
entrez: 19 5 2021
pubmed: 20 5 2021
medline: 20 5 2021
Statut: ppublish

Résumé

Anti-angiogenesis therapy is a novel treatment method for malignant tumors. Endothelial cell (EC) migration is an important part of angiogenesis. Dihydroartemisinin (DHA) exhibits strong anti-angiogenic and anti-EC migration effects; however, the underlying molecular mechanisms are yet to be elucidated. The TGF-β1/activin receptor-like kinase 5 (ALK5)/SMAD2 signaling pathway serves an important role in the regulation of migration. The present study aimed to explore the effects of DHA treatment on EC migration and the TGF-β1/ALK5/SMAD2 signaling pathway. The effects of DHA on human umbilical vein EC migration were assessed using wound healing and Transwell assays. The effects of DHA on the TGF-β1/ALK5/SMAD2 signaling pathway were detected using western blotting. DHA exhibited an inhibitory effect on EC migration in the wound healing and Transwell assays. DHA treatment upregulated the expression levels of ALK5 and increased the phosphorylation of SMAD2 in ECs. SB431542 rescued the inhibitory effect of DHA during EC migration. DHA inhibited EC migration via the TGF-β1/ALK5/SMAD2-dependent signaling pathway, and DHA may be a novel drug for the treatment of patients with malignant tumors.

Identifiants

pubmed: 34007318
doi: 10.3892/etm.2021.10141
pii: ETM-0-0-10141
pmc: PMC8120513
doi:

Types de publication

Journal Article

Langues

eng

Pagination

709

Informations de copyright

Copyright: © Guo et al.

Déclaration de conflit d'intérêts

The authors declare that they have no competing interests.

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Auteurs

Ling Guo (L)

Department of Cardiology, Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Shandong University, Jinan, Shandong 250014, P.R. China.
Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.

Xiaoqing Wen (X)

Department of Clinical Medicine, Weifang Medical University, Weifang, Shandong 261042, P.R. China.

Yinglong Hou (Y)

Department of Cardiology, Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Shandong University, Jinan, Shandong 250014, P.R. China.

Rong Sun (R)

Advanced Medical Research Institute, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250014, P.R. China.

Liang Zhang (L)

Shandong Provincial Key Laboratory of Animal Resistance Biology, Institute of Biomedical Sciences, College of Life Sciences, Shandong Normal University, Jinan, Shandong 250014, P.R. China.

Fuhong Liu (F)

Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.

Ju Liu (J)

Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.

Classifications MeSH