Role of cGMP in hydrogen sulfide signaling

•H2S donors and endogenous H2S increase cGMP.•This is achieved by PDE inhibition, eNOS activation or increased NO bioavailability.•H2S is a non-selective PDE inhibitor.•Rate of H2S release determines the concentration of donor needed to increase cGMP.•Donors with faster release rates are more likely...

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Published inNitric oxide Vol. 46; pp. 7 - 13
Main Authors Bibli, Sofia-Iris, Yang, Guangdong, Zhou, Zongmin, Wang, Rui, Topouzis, Stavros, Papapetropoulos, Andreas
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 30.04.2015
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Abstract •H2S donors and endogenous H2S increase cGMP.•This is achieved by PDE inhibition, eNOS activation or increased NO bioavailability.•H2S is a non-selective PDE inhibitor.•Rate of H2S release determines the concentration of donor needed to increase cGMP.•Donors with faster release rates are more likely to exert their effects through cGMP. The importance of hydrogen sulfide (H2S) in physiology and disease is being increasingly recognized in recent years. Unlike nitric oxide (NO) that signals mainly through soluble guanyl cyclase (sGC)/cGMP, H2S is more promiscuous, affecting multiple pathways. It interacts with ion channels, enzymes, transcription factors and receptors. It was originally reported that H2S does not alter the levels of cyclic nucleotides. More recent publications, however, have shown increases in intracellular cGMP following exposure of cells or tissues to exogenously administered or endogenously produced H2S. Herein, we discuss the evidence for the participation of cGMP in H2S signaling and reconcile the seemingly divergent results presented in the literature on the role of this cyclic nucleotide in the biological actions of H2S.
AbstractList The importance of hydrogen sulfide (H2S) in physiology and disease is being increasingly recognized in recent years. Unlike nitric oxide (NO) that signals mainly through soluble guanyl cyclase (sGC)/cGMP, H2S is more promiscuous, affecting multiple pathways. It interacts with ion channels, enzymes, transcription factors and receptors. It was originally reported that H2S does not alter the levels of cyclic nucleotides. More recent publications, however, have shown increases in intracellular cGMP following exposure of cells or tissues to exogenously administered or endogenously produced H2S. Herein, we discuss the evidence for the participation of cGMP in H2S signaling and reconcile the seemingly divergent results presented in the literature on the role of this cyclic nucleotide in the biological actions of H2S.The importance of hydrogen sulfide (H2S) in physiology and disease is being increasingly recognized in recent years. Unlike nitric oxide (NO) that signals mainly through soluble guanyl cyclase (sGC)/cGMP, H2S is more promiscuous, affecting multiple pathways. It interacts with ion channels, enzymes, transcription factors and receptors. It was originally reported that H2S does not alter the levels of cyclic nucleotides. More recent publications, however, have shown increases in intracellular cGMP following exposure of cells or tissues to exogenously administered or endogenously produced H2S. Herein, we discuss the evidence for the participation of cGMP in H2S signaling and reconcile the seemingly divergent results presented in the literature on the role of this cyclic nucleotide in the biological actions of H2S.
The importance of hydrogen sulfide (H2S) in physiology and disease is being increasingly recognized in recent years. Unlike nitric oxide (NO) that signals mainly through soluble guanyl cyclase (sGC)/cGMP, H2S is more promiscuous, affecting multiple pathways. It interacts with ion channels, enzymes, transcription factors and receptors. It was originally reported that H2S does not alter the levels of cyclic nucleotides. More recent publications, however, have shown increases in intracellular cGMP following exposure of cells or tissues to exogenously administered or endogenously produced H2S. Herein, we discuss the evidence for the participation of cGMP in H2S signaling and reconcile the seemingly divergent results presented in the literature on the role of this cyclic nucleotide in the biological actions of H2S.
•H2S donors and endogenous H2S increase cGMP.•This is achieved by PDE inhibition, eNOS activation or increased NO bioavailability.•H2S is a non-selective PDE inhibitor.•Rate of H2S release determines the concentration of donor needed to increase cGMP.•Donors with faster release rates are more likely to exert their effects through cGMP. The importance of hydrogen sulfide (H2S) in physiology and disease is being increasingly recognized in recent years. Unlike nitric oxide (NO) that signals mainly through soluble guanyl cyclase (sGC)/cGMP, H2S is more promiscuous, affecting multiple pathways. It interacts with ion channels, enzymes, transcription factors and receptors. It was originally reported that H2S does not alter the levels of cyclic nucleotides. More recent publications, however, have shown increases in intracellular cGMP following exposure of cells or tissues to exogenously administered or endogenously produced H2S. Herein, we discuss the evidence for the participation of cGMP in H2S signaling and reconcile the seemingly divergent results presented in the literature on the role of this cyclic nucleotide in the biological actions of H2S.
Author Bibli, Sofia-Iris
Topouzis, Stavros
Zhou, Zongmin
Papapetropoulos, Andreas
Yang, Guangdong
Wang, Rui
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Keywords Hydrogen sulfide
Relaxation
Angiogenesis
cGMP
PKG
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Snippet •H2S donors and endogenous H2S increase cGMP.•This is achieved by PDE inhibition, eNOS activation or increased NO bioavailability.•H2S is a non-selective PDE...
The importance of hydrogen sulfide (H2S) in physiology and disease is being increasingly recognized in recent years. Unlike nitric oxide (NO) that signals...
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SubjectTerms Angiogenesis
Animals
cGMP
Cyclic GMP - chemistry
Cyclic GMP - metabolism
Humans
Hydrogen sulfide
Hydrogen Sulfide - chemistry
Hydrogen Sulfide - metabolism
Mice
PKG
Relaxation
Signal Transduction
Title Role of cGMP in hydrogen sulfide signaling
URI https://dx.doi.org/10.1016/j.niox.2014.12.004
https://www.ncbi.nlm.nih.gov/pubmed/25553675
https://www.proquest.com/docview/1677889083
Volume 46
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