scholarly journals AP39, a novel mitochondria-targeted hydrogen sulfide donor, stimulates cellular bioenergetics, exerts cytoprotective effects and protects against the loss of mitochondrial DNA integrity in oxidatively stressed endothelial cells in vitro

Nitric Oxide ◽  
2014 ◽  
Vol 41 ◽  
pp. 120-130 ◽  
Author(s):  
Bartosz Szczesny ◽  
Katalin Módis ◽  
Kazunori Yanagi ◽  
Ciro Coletta ◽  
Sophie Le Trionnaire ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mitochondrial Dna ◽  
Hydrogen Sulfide ◽  
Dna Integrity ◽  
Cellular Bioenergetics

scholarly journals The novel mitochondria-targeted hydrogen sulfide (H 2 S) donors AP123 and AP39 protect against hyperglycemic injury in microvascular endothelial cells in vitro

2016 ◽  
Vol 113 ◽  
pp. 186-198 ◽  
Author(s):  
Domokos Gerő ◽  
Roberta Torregrossa ◽  
Alexis Perry ◽  
Alicia Waters ◽  
Sophie Le-Trionnaire ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Hydrogen Sulfide ◽  
Microvascular Endothelial Cells ◽  
The Novel ◽  
Microvascular Endothelial

P35 Cystathionine-β-synthase (CBS)-derived hydrogen sulfide (H2S) supports cellular bioenergetics in colon cancer cells in vitro

Nitric Oxide ◽  
2013 ◽  
Vol 31 ◽  
pp. S50 ◽  
Author(s):  
Katalin Módis ◽  
Ciro Coletta ◽  
Celia Chao ◽  
Andreas Papapetropoulos ◽  
Mark Hellmich ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Hydrogen Sulfide ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Cellular Bioenergetics

scholarly journals Selenium-Binding Protein 1 (SELENBP1) Supports Hydrogen Sulfide Biosynthesis and Adipogenesis

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 361 ◽  
Author(s):  
Elisa B. Randi ◽  
Giovanna Casili ◽  
Simona Jacquemai ◽  
Csaba Szabo
Keyword(s):  
Cell Proliferation ◽  
Hydrogen Sulfide ◽  
Lipid Accumulation ◽  
Intracellular Signaling ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Mitochondrial Activity ◽  
Knock Down ◽  
Cellular Bioenergetics

Hydrogen sulfide (H2S), a mammalian gasotransmitter, is involved in the regulation of a variety of fundamental processes including intracellular signaling, cellular bioenergetics, cell proliferation, and cell differentiation. Cystathionine γ-lyase (CSE), cystathionine β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) are currently considered the three principal mammalian H2S-generating enzymes. However, recently, a fourth H2S-producing enzyme, selenium-binding-protein 1 (SELENBP1), has also been identified. The cellular regulatory role(s) of SELENBP1 are incompletely understood. The current study investigated whether SELENBP1 plays a role in the regulation of adipocyte differentiation in vitro. 3T3-L1 preadipocytes with or without SELENBP1 knock-down were subjected to differentiation-inducing conditions, and H2S production, cellular lipid accumulation, cell proliferation, and mitochondrial activity were quantified. Adipocyte differentiation was associated with an upregulation of H2S biosynthesis. SELENBP1 silencing decreased cellular H2S levels, suppressed the expression of the three “classical” H2S-producing enzymes (CBS, CSE, and 3-MST) and significantly suppressed adipocyte differentiation. Treatment of SELENBP1 knock-down cells with the H2S donor GYY4137 partially restored lipid accumulation, increased cellular H2S levels, and exerted a bell-shaped effect on cellular bioenergetics (enhancement at 1 and 3 mM, and inhibition at 6 mM). We conclude that SELENBP1 in adipocytes (1) contributes to H2S biosynthesis and (2) acts as an endogenous stimulator of adipocyte differentiation.

The role of hydrogen sulfide in the adherence of endothelial cells in vitro

Nitric Oxide ◽  
2015 ◽  
Vol 47 ◽  
pp. S59
Author(s):  
Panagiotis Panopoulos ◽  
C. Malakis ◽  
Andreas Papapetropoulos ◽  
Stavros Topouzis
Keyword(s):  
Endothelial Cells ◽  
Hydrogen Sulfide

Hydrogen Sulfide: A Supporter of Mitochondrial DNA Repair and Cellular Bioenergetics in Lung CancerCells

2015 ◽  
Vol 87 ◽  
pp. S73
Author(s):  
Bartosz Szczesny ◽  
Michela Marcatti ◽  
Attila Brunyanszki ◽  
Mark R. Hellmich ◽  
Csaba Szabo
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dna ◽  
Hydrogen Sulfide ◽  
Mitochondrial Dna Repair ◽  
Cellular Bioenergetics

Ultrastructural studies on the interaction of haemophilus influenzae with human endothelial cells in vitro

1990 ◽  
Vol 48 (3) ◽  
pp. 636-637
Author(s):  
D.J.P. Ferguson ◽  
M. Virji ◽  
H. Kayhty ◽  
E.R. Moxon
Keyword(s):  
Endothelial Cells ◽  
Haemophilus Influenzae ◽  
Intercellular Junctions ◽  
Blood Stream ◽  
Ultrastructural Studies ◽  
Endothelial Barriers ◽  
Serotype B ◽  
Meningitis In Children ◽  
Respiratory Epithelial

Haemophilus influenzae is a human pathogen which causes meningitis in children. Systemic H. influenzae infection is largely confined to encapsulated serotype b organisms and is a major cause of meningitis in the U.K. and elsewhere. However, the pathogenesis of the disease is still poorly understood. Studies in the infant rat model, in which intranasal challenge results in bacteraemia, have shown that H. influenzae enters submucosal tissues and disseminates to the blood stream within minutes. The rapidity of these events suggests that H. influenzae penetrates both respiratory epithelial and endothelial barriers with great efficiency. It is not known whether the bacteria penetrate via the intercellular junctions, are translocated within the cells or carried across the cellular barrier in 'trojan horse' fashion within phagocytes. In the present studies, we have challenged cultured human umbilical cord_vein endothelial cells (HUVECs) with both capsulated (b+) and capsule-deficient (b-) isogenic variants of one strain of H. influenzae in order to investigate the interaction between the bacteria and HUVEC and the effect of the capsule.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

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