Capture and Visualization of Hydrogen Sulfide by a Fluorescent Probe

Liu, Chunrong; Pan, Jia; Sheng, Li; Zhao, Yu; Wu, Lizhong; Berkman, Clifford E.; Whorton, A. R.; Xian, Ming

doi:10.1002/anie.201104305

Cited by 545 publications

(282 citation statements)

References 25 publications

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“…Recently, the basal concentrations of H 2 S in tissues have been measured and found to be much lower than those previously reported (18,24,36). During the preparation of this manuscript, H 2 S-sensitive fluorescence probes have been reported from several laboratories (38,39,50,52,55). These probes may enable us to detect the sites at which H 2 S is released in real time and assess the local concentrations of H 2 S.…”

Section: Introductionmentioning

confidence: 90%

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Kimura

Shibuya²,

Kimura³

2012

Antioxidants & Redox Signaling

260

190

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Significance: Accumulating evidence shows that hydrogen sulfide may function as a signaling molecule in processes such as neuromodulation in the brain and smooth muscle relaxation in the vascular system. It also has a cytoprotective effect, since it can protect neurons and cardiac muscle from oxidative stress and ischemiareperfusion injury, respectively. Hydrogen sulfide can also modulate inflammation, insulin release, and angiogenesis. Recent Advances: The regulation of the activity of 3-mercaptopyruvate sulfur transferase (3MST) along with cysteine aminotransferase (CAT), one of the H 2 S producing pathways, has been demonstrated. The production of H 2 S by the pathway, which is regulated by Ca 2+ and facilitated by thioredoxin and dihydrolipoic acid, is also involved in H 2 S signaling as well as cytoprotection. Sulfur hydration of proteins by H 2 S has been proposed to modulate protein functions. H 2 S-sensitive fluorescent probes, which enable us to measure the localization of H 2 S in real time, have been developed. Critical Issues: The basal concentrations of H 2 S have recently been measured and found to be much lower than those initially reported. However, the concentration of H 2 S reached in stimulated cells, as well as the regulation of H 2 S producing enzymes is not well understood. It has been proposed that some of the effects of H 2 S on the regulation of enzymes and receptors might be explained through the properties of sulfane sulfur (S 0 ), another form of active sulfur. Future Directions: The determination of H 2 S concentrations in activated cells using new methods including H 2 S-sensitive fluorescent probes, as well as the investigation of the effects of H 2 S using specific inhibitors, may provide better understanding of the physiological function of this molecule. Clarifying mechanisms of H 2 S activity may also facilitate the development of new therapeutic compounds. Antioxid. Redox Signal. 17, 45-57.

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Section: Introductionmentioning

confidence: 90%

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Kimura

Shibuya²,

Kimura³

2012

Antioxidants & Redox Signaling

260

190

View full text Add to dashboard Cite

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“…Intracellular free H 2 S levels were determined using the H 2 S fluorescent probe (WSP-1; kindly provided by Professor Ming Xian at the Department of Chemistry, Washington State University, Pullman, WA, USA), as previously described (19,20) and the chemical equation is presented in Fig. 1.…”

Section: Measurement Of Intracellular H 2 S Contentmentioning

confidence: 99%

H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2

Liu

Cai

et al. 2013

International Journal of Molecular Medicine

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Abstract. The hypoxia-induced proliferation of pulmonary artery smooth muscle cells (PASMCs) is the main cause of pulmonary arterial hypertension (PAH), in which oxidative stress, cyclooxygenase (COX)-2 and hydrogen sulfide (H 2 S) all play an important role. In the present study, we aimed to examine the effects of H 2 S on the hypoxia-induced proliferation of human PASMCs (HPASMCs) and to elucidate the underlying mechanisms. The HPASMCs were treated with cobalt chloride (CoCl 2 ), a hypoxia-mimicking agent, to establish a cellular model of hypoxic PAH. Prior to treatment with CoCl 2 , the cells were pre-conditioned with sodium hydrosulfide (NaHS), a donor of H 2 S. Cell proliferation, reactive oxygen species (ROS) production, COX-2 expression, prostacyclin (also known as prostaglandin I2 or PGI 2 ) secretion and H 2 S levels were detected in the cells. The exposure of the HPASMCs to CoCl 2 markedly increased cell proliferation, accompanied by a decrease in COX-2 expression, PGI 2 secretion and H 2 S levels; however, the levels of ROS were not altered. Although the exogenous ROS donor, H 2 O 2 , triggered similar degrees of proliferation to CoCl 2 , the ROS scavenger, N-acetyl-L-cysteine (NAC), markedly abolished the H 2 O 2 -induced cell proliferation, as opposed to the CoCl 2 -induced proliferation. The CoCl 2 -induced proliferation of HPASMCs was suppressed by exogenously applied PGI 2 . The addition of H 2 S (NaHS) attenuated the CoCl 2 -induced cell proliferation through the increase in the intercellular content of H 2 S. Importantly, the exposure of the cells to H 2 S suppressed the CoCl 2 -induced downregulation in COX-2 expression and PGI 2 secretion from the HPASMCs. In conclusion, the results from the current study suggest that H 2 S inhibits hypoxia-induced cell proliferation through the upregulation of COX-2/PGI 2 , as opposed to ROS.

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“…The main limitations of our chemistry stem from acidic cleavage (5% TFA/DCM) that precludes the presence of acid-labile groups (e.g., acetal) and the use of hydrogen sulfide gas. Hydrogen sulfide in solution is a reducing agent that reduces azide functions in water [16], and is also a nucleophilic species that reacts with disulfides [17].…”

Section: Synthesis On Resin: Scope and Limitationsmentioning

confidence: 99%

A CuAAC–Hydrazone–CuAAC Trifunctional Scaffold for the Solid-Phase Synthesis of Trimodal Compounds: Possibilities and Limitations

et al. 2015

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Abstract:We present a trifunctional scaffold designed for the solid-phase synthesis of trimodal compounds. This scaffold holds two alkyne arms in a free and TIPS-protected form for consecutive CuAAC (copper(I)-catalyzed azide-alkyne cycloaddition), one Fmoc-protected hydrazide arm for reaction with aldehydes, and one carboxylic acid arm with CF2 groups for attachment to the resin and 19 F-NMR quantification. This scaffold was attached to a resin and derivatized with model azides and aliphatic, electron-rich or electron-poor aromatic aldehydes. We identified several limitations of the scaffold caused by the instability of hydrazones in acidic conditions, in the presence of copper during CuAAC, and when copper accumulated in the resin. We successfully overcame these drawbacks by optimizing synthetic conditions for the derivatization of the scaffold with aromatic aldehydes. Overall, the new trifunctional scaffold combines CuAAC and hydrazone chemistries, offering a broader chemical space for the development of bioactive compounds.

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Capture and Visualization of Hydrogen Sulfide by a Fluorescent Probe

Cited by 545 publications

References 25 publications

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

Hydrogen Sulfide Is a Signaling Molecule and a Cytoprotectant

H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2

A CuAAC–Hydrazone–CuAAC Trifunctional Scaffold for the Solid-Phase Synthesis of Trimodal Compounds: Possibilities and Limitations

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