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Hydrogen sulfide metabolism regulates endothelial solute barrier function.
Shuai Yuan1, Sibile Pardue2, Xinggui Shen2
1Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA 71103, USA.
Redox Biology
|August 24, 2016
Summary
Hydrogen sulfide (H2S) and its metabolite polysulfides impact endothelial barrier function. Polysulfides, not free H2S, rapidly increase permeability by disrupting junction proteins.
Area of Science:
- Cardiovascular Physiology
- Cell Biology
- Biochemistry
Background:
- Hydrogen sulfide (H2S) is a key gasotransmitter in the cardiovascular system.
- H2S can be oxidized to biologically active polysulfides.
- The effect of H2S on endothelial barrier function was previously unknown.
Purpose of the Study:
- To investigate the impact of H2S and its metabolites on endothelial permeability.
- To determine the role of exogenous and endogenous H2S in regulating endothelial barrier function.
Main Methods:
- In vitro assessment of endothelial permeability using albumin flux and transendothelial electrical resistance.
- In vivo evaluation of permeability using the Miles assay.
- Utilized H2S donors, mouse aortic endothelial cells (MAECs) from wild type and CSE-deficient mice, and siRNA knockdown.
Main Results:
- Polysulfide donors rapidly increased albumin flux, while free sulfide donors had a delayed and concentration-dependent effect.
- Increased permeability correlated with disrupted claudin 5 and VE-cadherin, and actin stress fiber formation.
- CSE deficiency enhanced endothelial barrier function and reduced endogenous sulfane sulfur; genetic deficiency blunted VEGF-induced hyperpermeability.
Conclusions:
- Endothelial solute permeability is regulated by H2S bioavailability, with polysulfides playing a prominent role.
- Endogenous H2S, produced by cystathionine γ-lyase (CSE), is crucial for maintaining endothelial barrier integrity.
- Polysulfides are key mediators of H2S-induced changes in endothelial permeability.
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