ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine: role of BK channels.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
- Complex Pathophysiology of Acute Kidney Injury (AKI) in Aging: Epigenetic Regulation, Matrix Remodeling, and the Healing Effects of HBiomolecules · 2024Review
- Review
- Cerebral Ischemia/Reperfusion Injury and Pharmacologic Preconditioning as a Means to Reduce Stroke-induced Inflammation and Damage.Neurochemical research · 2022Review
- Involvement of 3',5'-cyclic inosine monophosphate in cystathionine γ-lyase-dependent regulation of the vascular tone.British journal of pharmacology · 2021Article
- Elevated postischemic tissue injury and leukocyte-endothelial adhesive interactions in mice with global deficiency in caveolin-2: role of PAI-1.American journal of physiology. Heart and circulatory physiology · 2021Article
- Basic Pharmacological Characterization of EV-34, a New HMolecules (Basel, Switzerland) · 2021Article
- Hydrogen sulphide ameliorates dopamine-induced astrocytic inflammation and neurodegeneration in minimal hepatic encephalopathy.Journal of cellular and molecular medicine · 2020Article
- Regulation of carbohydrate metabolism by nitric oxide and hydrogen sulfide: Implications in diabetes.Biochemical pharmacology · 2020Review
- Chlorinated Lipids Elicit Inflammatory Responses in vitro and in vivo.Shock (Augusta, Ga.) · 2019Article
- Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide.Frontiers in pharmacology · 2019Review
- Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury.Scientific reports · 2018Article
- Regulation of vascular tone homeostasis by NO and HBiochemical pharmacology · 2018Review
- Preconditioning with the BKAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- HFrontiers in pharmacology · 2017Review
- Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels.American journal of physiology. Heart and circulatory physiology · 2016Article
- Soluble guanylate cyclase activation during ischemic injury in mice protects against postischemic inflammation at the mitochondrial level.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- The role of H2S bioavailability in endothelial dysfunction.Trends in pharmacological sciences · 2015Review
- Lean and Obese Coronary Perivascular Adipose Tissue Impairs Vasodilation via Differential Inhibition of Vascular Smooth Muscle K+ Channels.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Modes of physiologic H2S signaling in the brain and peripheral tissues.Antioxidants & redox signaling · 2015Review
- NaHS Protects Cochlear Hair Cells from Gentamicin-Induced Ototoxicity by Inhibiting the Mitochondrial Apoptosis Pathway.PloS one · 2015Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The objectives of this study were to determine the role of calcium-activated, small (SK), intermediate (IK), and large (BK) conductance potassium channels in initiating the development of an anti-inflammatory phenotype elicited by preconditioning with an exogenous hydrogen sulfide (H(2)S) donor, sodium hydrosulfide (NaHS). Intravital microscopy was used to visualize rolling and firmly adherent leukocytes in vessels of the small intestine of mice preconditioned with NaHS (in the absence and presence of SK, IK, and BK channel inhibitors, apamin, TRAM-34, and paxilline, respectively) or SK/IK (NS-309) or BK channel activators (NS-1619) 24 h before ischemia-reperfusion (I/R). I/R induced marked increases in leukocyte rolling and adhesion, effects that were largely abolished by preconditioning with NaHS, NS-309, or NS-1619. The postischemic anti-inflammatory effects of NaHS-induced preconditioning were mitigated by BKB channel inhibitor treatment coincident with NaHS, but not by apamin or TRAM-34, 24 h before I/R. Confocal imaging and immunohistochemistry were used to demonstrate the presence of BKα subunit staining in both endothelial and vascular smooth muscle cells of isolated, pressurized mesenteric venules. Using patch-clamp techniques, we found that BK channels in cultured endothelial cells were activated after exposure to NaHS. Bath application of the same concentration of NaHS used in preconditioning protocols led to a rapid increase in a whole cell K(+) current; specifically, the component of K(+) current blocked by the selective BK channel antagonist iberiotoxin. The activation of BK current by NaHS could also be demonstrated in single channel recording mode where it was independent of a change in intracellular Ca(+) concentration. Our data are consistent with the concept that H(2)S induces the development of an anti-adhesive state in I/R in part mediated by a BK channel-dependent mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.