scholarly journals Quantitative Monitoring and Visualization of Hydrogen Sulfide In Vivo Using a Luminescent Probe Based on a Ruthenium(II) Complex

2018 ◽  
Vol 57 (15) ◽  
pp. 3999-4004 ◽  
Author(s):  
Zhongbo Du ◽  
Bo Song ◽  
Wenzhu Zhang ◽  
Chengchen Duan ◽  
Yong-Lei Wang ◽  
...  
2018 ◽  
Vol 130 (15) ◽  
pp. 4063-4068 ◽  
Author(s):  
Zhongbo Du ◽  
Bo Song ◽  
Wenzhu Zhang ◽  
Chengchen Duan ◽  
Yong-Lei Wang ◽  
...  

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  

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.


1991 ◽  
Vol 65 (04) ◽  
pp. 425-431 ◽  
Author(s):  
F Stockmans ◽  
H Deckmyn ◽  
J Gruwez ◽  
J Vermylen ◽  
R Acland

SummaryA new in vivo method to study the size and dynamics of a growing mural thrombus was set up in the rat femoral vein. The method uses a standardized crush injury to induce a thrombus, and a newly developed transilluminator combined with digital analysis of video recordings. Thrombi in this model formed rapidly, reaching a maximum size 391 ± 35 sec following injury, after which they degraded with a half-life of 197 ± 31 sec. Histological examination indicated that the thrombi consisted mainly of platelets. The quantitative nature of the transillumination technique was demonstrated by simultaneous measurement of the incorporation of 111In labeled platelets into the thrombus. Thrombus formation, studied at 30 min interval in both femoral veins, showed satisfactory reproducibility overall and within a given animalWith this method we were able to induce a thrombus using a clinically relevant injury and to monitor continuously and reproducibly the kinetics of thrombus formation in a vessel of clinically and surgically relevant size


2019 ◽  
Author(s):  
Fangfang Cai ◽  
Nini Cao ◽  
Xiangyu Zhang ◽  
Jia Liu ◽  
Huangru Xu ◽  
...  

2020 ◽  
Vol 8 (S1) ◽  
Author(s):  
Tamara Merz ◽  
Nicole Denoix ◽  
Martin Wepler ◽  
Holger Gäßler ◽  
David A. C. Messerer ◽  
...  

AbstractThis review addresses the plausibility of hydrogen sulfide (H2S) therapy for acute lung injury (ALI) and circulatory shock, by contrasting the promising preclinical results to the present clinical reality. The review discusses how the narrow therapeutic window and width, and potentially toxic effects, the route, dosing, and timing of administration all have to be balanced out very carefully. The development of standardized methods to determine in vitro and in vivo H2S concentrations, and the pharmacokinetics and pharmacodynamics of H2S-releasing compounds is a necessity to facilitate the safety of H2S-based therapies. We suggest the potential of exploiting already clinically approved compounds, which are known or unknown H2S donors, as a surrogate strategy.


2021 ◽  
pp. 109451
Author(s):  
Jie Li ◽  
Zhe Su ◽  
Changmin Yu ◽  
Yan Yuan ◽  
Qiong Wu ◽  
...  

2012 ◽  
Vol 32 (12) ◽  
pp. 2884-2891 ◽  
Author(s):  
Joachim Pircher ◽  
Franziska Fochler ◽  
Thomas Czermak ◽  
Hanna Mannell ◽  
Bjoern F. Kraemer ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Zhuping Jin ◽  
Yanxi Pei

Recently, overwhelming evidence has proven that hydrogen sulfide (H2S), which was identified as a gasotransmitter in animals, plays important roles in diverse physiological processes in plants as well. With the discovery and systematic classification of the enzymes producing H2Sin vivo, a better understanding of the mechanisms by which H2S influences plant responses to various stimuli was reached. There are many functions of H2S, including the modulation of defense responses and plant growth and development, as well as the regulation of senescence and maturation. Additionally, mounting evidence indicates that H2S signaling interacts with plant hormones, hydrogen peroxide, nitric oxide, carbon monoxide, and other molecules in signaling pathways.


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