Sodium thiosulfate, a source of hydrogen sulfide, stimulates endothelial cell proliferation and neovascularization.
Details
Serval ID
serval:BIB_B3BEAE5B7756
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Sodium thiosulfate, a source of hydrogen sulfide, stimulates endothelial cell proliferation and neovascularization.
Journal
Frontiers in cardiovascular medicine
ISSN
2297-055X (Print)
ISSN-L
2297-055X
Publication state
Published
Issued date
2022
Peer-reviewed
Oui
Volume
9
Pages
965965
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Publication Status: epublish
Abstract
Therapies to accelerate vascular repair are currently lacking. Pre-clinical studies suggest that hydrogen sulfide (H <sub>2</sub> S), an endogenous gasotransmitter, promotes angiogenesis. Here, we hypothesized that sodium thiosulfate (STS), a clinically relevant source of H <sub>2</sub> S, would stimulate angiogenesis and vascular repair. STS stimulated neovascularization in WT and LDLR receptor knockout mice following hindlimb ischemia as evidenced by increased leg perfusion assessed by laser Doppler imaging, and capillary density in the gastrocnemius muscle. STS also promoted VEGF-dependent angiogenesis in matrigel plugs in vivo and in the chorioallantoic membrane of chick embryos. In vitro, STS and NaHS stimulated human umbilical vein endothelial cell (HUVEC) migration and proliferation. Seahorse experiments further revealed that STS inhibited mitochondrial respiration and promoted glycolysis in HUVEC. The effect of STS on migration and proliferation was glycolysis-dependent. STS probably acts through metabolic reprogramming of endothelial cells toward a more proliferative glycolytic state. These findings may hold broad clinical implications for patients suffering from vascular occlusive diseases.
Keywords
angiogenesis, arteriogenesis, endothelial cells, hydrogen sulfide, inflammation, peripheral arterial disease, thiosulfate
Pubmed
Web of science
Open Access
Yes
Create date
02/11/2022 10:21
Last modification date
08/08/2024 7:27