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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Sharina, Iraida Asimakopoulou, Antonia Papapetropoulos, Andreas Szabo, Csaba Módis, Katalin Martin, Emil Coletta, Ciro Panopoulos, Panagiotis Olah, Gabor Gerö, Domokos Erdelyi, Katalin |
| Description | Author Affiliation: Coletta C ( Department of Anesthesiology, University of Texas Medical Branch and Shriners Burns Hospital for Children, Galveston, TX 77555, USA.); |
| Abstract | Hydrogen sulfide $(H_{2}S)$ is a unique gasotransmitter, with regulatory roles in the cardiovascular, nervous, and immune systems. Some of the vascular actions of $H_{2}S$ (stimulation of angiogenesis, relaxation of vascular smooth muscle) resemble those of nitric oxide (NO). Although it was generally assumed that $H_{2}S$ and NO exert their effects via separate pathways, the results of the current study show that $H_{2}S$ and NO are mutually required to elicit angiogenesis and vasodilatation. Exposure of endothelial cells to $H_{2}S$ increases intracellular cyclic guanosine 5′-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Inhibition of endothelial isoform of NO synthase (eNOS) or PKG-I abolishes the $H_{2}S-stimulated$ angiogenic response, and attenuated $H_{2}S-stimulated$ vasorelaxation, demonstrating the requirement of NO in vascular $H_{2}S$ signaling. Conversely, silencing of the $H_{2}S-producing$ enzyme cystathionine-γ-lyase abolishes NO-stimulated cGMP accumulation and angiogenesis and attenuates the acetylcholine-induced vasorelaxation, indicating a partial requirement of $H_{2}S$ in the vascular activity of NO. The actions of $H_{2}S$ and NO converge at cGMP; though $H_{2}S$ does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitory effect on PDE5, thereby delaying the degradation of cGMP. $H_{2}S$ also activates PI3K/Akt, and increases eNOS phosphorylation at its activating site S1177. The cooperative action of the two gasotransmitters on increasing and maintaining intracellular cGMP is essential for PKG activation and angiogenesis and vasorelaxation. $H_{2}S-induced$ wound healing and microvessel growth in matrigel plugs is suppressed by pharmacological inhibition or genetic ablation of eNOS. Thus, NO and $H_{2}S$ are mutually required for the physiological control of vascular function. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 23 |
| Volume Number | 109 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2012-06-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Endothelial Cells Metabolism Gene Expression Regulation Drug Effects Hydrogen Sulfide Pharmacology Neovascularization, Physiologic Physiology Nitric Oxide Vasodilation Analysis Of Variance Animals Blotting, Western Cell Adhesion Molecules Cell Line Collagen Cyclic GMP Cyclic GMP-Dependent Protein Kinases Cystathionine Gamma-Lyase Drug Combinations Laminin Mice Microfilament Proteins Nitric Oxide Synthase Type III Phosphoproteins Phosphorylation Proteoglycans Rats, Sprague-Dawley Wound Healing Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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