The Effect of Certain Conditions in the Regulation of Cystathionine γ-Lyase by Exogenous Hydrogen Sulfide in Mammalian Cells

  title={The Effect of Certain Conditions in the Regulation of Cystathionine $\gamma$-Lyase by Exogenous Hydrogen Sulfide in Mammalian Cells},
  author={Maoxian Wang and Zhanyun Guo and Shilong Wang},
  journal={Biochemical Genetics},
Cystathionine γ-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using l-cysteine or l-homocysteine as a substrate. The regulatory mechanism of CSE by exogenous H2S remains unknown. The transcription and expression of the CSE gene regulated by exogenous H2S at approximately physiologic concentrations was investigated using luciferase assay, Western blotting, and quantitative RT-PCR. The results revealed… 

Human Cystathionine γ-Lyase Is Inhibited by s-Nitrosation: A New Crosstalk Mechanism between NO and H2S

H2S production by recombinant human CSE was found to be inhibited by the physiological nitrosating agent s-nitrosoglutathione (GSNO), while reduced glutathione had no effect, highlighting a new mechanism of crosstalk between gasotransmitters.

Exogenous H2S regulates the expression of cystathionine gamma-lyase in HUVECs during hypoxia

Findings suggest that vascular endothelial cells can respond to changes in H2S concentration in the blood during hypoxia, and this work examined the regulatory effect of 100 μM H1N1 on the transcription and expression of CSE in HUVECs duringhypoxia.

The H2S Donor NaHS Changes the Expression Pattern of H2S-Producing Enzymes after Myocardial Infarction

Exogenous H 2S treatment changed the expressions of three H2S-producing enzymes and H1S levels after MI, suggesting a new and indirect regulatory mechanism for H2s production and its contribution to cardiac protection.

Chemical Biology of Hydropersulfides and Related Species: Possible Roles in Cellular Protection and Redox Signaling.

It appears that H2S and RSSH are intimately linked in biological systems and likely to be mutually inclusive, and it remains possible that hydropersulfides are the biological effectors, and H 2S serves, to a certain extent, as a marker for persulfides and polysulfides.

The DR1-CSE/H2S system inhibits renal fibrosis by downregulating the ERK1/2 signaling pathway in diabetic mice

The findings suggested that the DR1-CSE/H2S pathway activation attenuated diabetic MC proliferation and extracellular matrix deposition by downregulating the ERK1/2 signaling pathway.

Dopamine 1 receptors inhibit apoptosis via activating CSE/H2S pathway in high glucose‐induced vascular endothelial cells

It is found that DR1 upregulates the CSE/H2S pathway by increasing the [Ca2+]i, which inhibits HG‐induced apoptosis via downregulating NF‐κB/IκBα pathway in vascular endothelial cells.

Hydrogen Sulfide Inhibits Ferroptosis in Cardiomyocytes to Protect Cardiac Function in Aging Rats

It is demonstrated that cardiac dysfunction associated with aging was closely related to decreased endogenous H2S levels and cardiomyocyte ferroptosis, and protected cardiac function in aging rats.

Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress

It is suggested that H2S may alleviate rat aorta VC by inhibiting ERS, providing new target and perspective for prevention and treatment of VC.

Characterization of zofenoprilat as an inducer of functional angiogenesis through increased H2S availability

The objective of this study was to evaluate whether zofenoprilat‐induced angiogenesis was due to increased H2S availability.



Cystathionine γ-Lyase Overexpression Inhibits Cell Proliferation via a H2S-dependent Modulation of ERK1/2 Phosphorylation and p21Cip/WAK-1*

The hypothesis that endogenously produced H2S may play a fundamental role in cell proliferation and survival is supported.

Hydrogen sulfide is a novel mediator of lipopolysaccharide‐induced inflammation in the mouse

  • Ling-Xia LiM. Bhatia P. Moore
  • Medicine, Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2005
It is suggested that H2S exhibits proinflammatory activity in endotoxic shock and a new approach to the development of novel drugs for this condition is suggested.

Hydrogen sulfide: its production and functions

It is demonstrated that a third H2S‐producing enzyme, 3‐mercaptopyruvate sulfurtransferase (3MST), is expressed in neurons and vascular endothelium, which reduces reactive oxygen species generated in these organelles and protects neurons from oxidative stress by reinstating the reduced glutathione levels.

3-Mercaptopyruvate sulfurtransferase produces hydrogen sulfide and bound sulfane sulfur in the brain.

3-mercaptopyruvate sulfurtransferase (3MST) in combination with Cysteine aminotransferase (CAT) produces H(2)S from cysteine, and the levels of bound sulfane sulfur are greatly increased in the cells expressing 3MST and CAT but not increased in cells expressing functionally defective mutant enzymes.

L-cysteine inhibits insulin release from the pancreatic beta-cell: possible involvement of metabolic production of hydrogen sulfide, a novel gasotransmitter.

It is suggested here that L-cysteine inhibits insulin release via multiple actions on the insulin secretory process through H(2)S production, which may participate in the deterioration of insulin release in this disease.

Pro‐apoptotic effect of endogenous H2S on human aorta smooth muscle cells

It is demonstrated that overexpression of CSE stimulates SMC apoptosis due to an increased endogenous production of H2S, which may provide a novel therapeutic approach in treating vascular diseases linked to abnormal cellular proliferation and vascular remodeling.

The possible role of hydrogen sulfide as an endogenous smooth muscle relaxant in synergy with nitric oxide.

Hydrogen sulfide (H2S), which is well known as a toxic gas, is produced endogenously in mammalian tissues from L-cysteine mainly by two pyridoxal-5'-phosphate-dependent enzymes, cystathionine

Hydrogen sulfide contributes to hypoxia-induced radioresistance on hepatoma cells.

It is demonstrated that H(2)S contributed to hypoxia-induced radioresistance probably via the opening of K(+)(ATP) channels, which suggests that the endogenous H( 2)S synthase could be a potential radiotherapeutic target for a hypoxic tumor.