ArticleBritish journal of pharmacology2008
H2S-donating sildenafil (ACS6) inhibits superoxide formation and gp91phox expression in arterial endothelial cells: role of protein kinases A and G.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 108 citations in OpenAlex.
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- Hydrogen sulfide and its potential as a possible therapeutic agent in male reproduction.Frontiers in endocrinology · 2024Review
- A novel, microvascular evaluation method and device for early diagnosis of peripheral artery disease and chronic limb-threatening ischemia in individuals with diabetes.Journal of vascular surgery cases and innovative techniques · 2023Article
- Pulmonary artery targeted therapy in treatment of COVID-19 related ARDS. Literature review.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021Article
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- The Role of Hydrogen Sulfide in Respiratory Diseases.Biomolecules · 2021Review
- Dynamic Function and Composition Shift in Circulating Innate Immune Cells in Hibernating Garden Dormice.Frontiers in physiology · 2021Article
- Hydrogen Sulfide as Potential RegulatoryInternational journal of molecular sciences · 2020Review
- The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art.International journal of molecular sciences · 2019Review
- Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers.Turkish journal of biology = Turk biyoloji dergisi · 2018Article
- International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of HPharmacological reviews · 2017Review
- Hydrogen sulfide stimulates CFTR in Xenopus oocytes by activation of the cAMP/PKA signalling axis.Scientific reports · 2017Article
- Hydrogen Sulfide Improves Endothelial Dysfunction via Downregulating BMP4/COX-2 Pathway in Rats with Hypertension.Oxidative medicine and cellular longevity · 2016Article
- The role of H2S bioavailability in endothelial dysfunction.Trends in pharmacological sciences · 2015Review
- Protective effects of hydrogen sulfide inhalation on oxidative stress in rats with cotton smoke inhalation-induced lung injury.Experimental and therapeutic medicine · 2015Article
- Hydrogen sulfide decreases β-adrenergic agonist-stimulated lung liquid clearance by inhibiting ENaC-mediated transepithelial sodium absorption.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Hydrogen sulfide: physiological properties and therapeutic potential in ischaemia.British journal of pharmacology · 2015Review
- Superoxide Mediates Depressive Effects Induced by Hydrogen Sulfide in Rostral Ventrolateral Medulla of Spontaneously Hypertensive Rats.Oxidative medicine and cellular longevity · 2015Article
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- Expression of concern
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeSuperoxide (O(2)(*-)), derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, is associated with acute respiratory distress syndrome (ARDS). NADPH oxidase activity and expression are blocked by nitric oxide (NO) and sildenafil. As another gas, hydrogen sulphide (H(2)S) is formed by blood vessels, the effect of sodium hydrosulphide (NaHS) and the H(2)S-donating derivative of sildenafil, ACS6, on O(2)(*-) formation and the expression of gp91(phox) (a catalytic subunit of NADPH oxidase) in porcine pulmonary arterial endothelial cells (PAECs) was investigated. EXPERIMENTAL APPROACH: PAECs were incubated with 10 ng mL(-1) tumour necrosis factor-alpha (TNFalpha) (+/-NaHS or ACS6), both of which released H(2)S, for 2 h or 16 h. O(2)(*-) was measured. Expression of gp91(phox) was measured by western blotting and the role of cyclic AMP (cAMP) and/or cyclic GMP was assessed using protein kinase inhibitors. KEY
resultsAfter either 2- or 16-h incubations, O(2)(*-) formation by PAECs was inhibited by NaHS or ACS6, with IC(50) values of about 10 nM and less than 1 nM, respectively. Both 100 nM NaHS and 1 nM ACS6 completely inhibited gp91(phox) expression induced by TNFalpha. The effects of NaHS were blocked by the inhibition of protein kinase A (PKA), but not PKG, and not by the inhibition of guanylyl cyclase. Effects of ACS6 were blocked by inhibition of both PKA and PKG. Both NaHS and ACS6 augmented cAMP formation. CONCLUSION AND IMPLICATIONS: H(2)S inhibited O(2)(*-) formation and upregulation of NADPH oxidase in PAECs through the adenylyl cyclase-PKA pathway. ACS6 may be effective in treating ARDS through both elevation of cAMP and inhibition of phosphodiesterase type 5 activity.
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