ArticleMolecular pharmacology2013
Hydrogen sulfide as an allosteric modulator of ATP-sensitive potassium channels in colonic inflammation.
Article in Molecular pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Gain-of-function mutations in KATP channel subunits compromise colonic tight junction integrity and epithelial homeostasis in murine models of Cantú syndrome.Frontiers in medicine · 2025Article
- Multiple beta cell-independent mechanisms drive hypoglycemia in Timothy syndrome.Nature communications · 2024Article
- Modulatory Impact of Oxidative Stress on Action Potentials in Pathophysiological States: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- Nitric oxide and ion channels mediate L-cysteine-induced inhibition of colonic smooth muscle contraction.Journal of muscle research and cell motility · 2024Article
- Hydrogen sulfide responsive nanoplatforms: Novel gas responsive drug delivery carriers for biomedical applications.Asian journal of pharmaceutical sciences · 2024Review
- Review
- Hydrogen Sulfide and its Interaction with Other Players in Inflammation.Advances in experimental medicine and biology · 2021Article
- Therapeutic importance of hydrogen sulfide in age-associated neurodegenerative diseases.Neural regeneration research · 2020Review
- An Indole Alkaloid Extracted fromGastroenterology research and practice · 2020Article
- Gasotransmitters in pregnancy: from conception to uterine involution.Biology of reproduction · 2019Review
- Mechanisms by which hydrogen sulfide attenuates muscle function following ischemia-reperfusion injury: effects on Akt signaling, mitochondrial function, and apoptosis.Journal of translational medicine · 2019Review
- Hydrogen sulfide inhibits Kir2 and Kir3 channels by decreasing sensitivity to the phospholipid phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of biological chemistry · 2018Article
- Augmentation of cGMP/PKG pathway and colonic motility by hydrogen sulfide.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Inhibition of RhoA/Rho kinase pathway and smooth muscle contraction by hydrogen sulfide.Pharmacology research & perspectives · 2017Article
- Vascular biology of hydrogen sulfide.American journal of physiology. Cell physiology · 2017Review
- HFrontiers in pharmacology · 2017Review
- S-sulfhydration as a cellular redox regulation.Bioscience reports · 2015Review
- ABCC9/SUR2 in the brain: Implications for hippocampal sclerosis of aging and a potential therapeutic target.Ageing research reviews · 2015Review
- Hydrogen sulfide-based therapeutics: exploiting a unique but ubiquitous gasotransmitter.Nature reviews. Drug discovery · 2015Review
- Interaction between hydrogen sulfide-induced sulfhydration and tyrosine nitration in the KATP channel complex.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The ATP-sensitive potassium channel (K(ATP)) in mouse colonic smooth muscle cell is a complex containing a pore-forming subunit (Kir6.1) and a sulfonylurea receptor subunit (SUR2B). These channels contribute to the cellular excitability of smooth muscle cells and hence regulate the motility patterns in the colon. Whole-cell voltage-clamp techniques were used to study the alterations in K(ATP) channels in smooth muscle cells in experimental colitis. Colonic inflammation was induced in BALB/C mice after intracolonic administration of trinitrobenzene sulfonic acid. K(ATP) currents were measured at a holding potential of -60 mV in high K(+) external solution. The concentration response to levcromakalim (LEVC), a K(ATP) channel opener, was significantly shifted to the left in the inflamed smooth-muscle cells. Both the potency and maximal currents induced by LEVC were enhanced in inflammation. The EC(50) values in control were 6259 nM (n = 10) and 422 nM (n = 8) in inflamed colon, and the maximal currents were 9.9 ± 0.71 pA/pF (60 μM) in control and 39.7 ± 8.8 pA/pF (3 μM) after inflammation. As was seen with LEVC, the potency and efficacy of sodium hydrogen sulfide (NaHS) (10-1000 μM) on K(ATP) currents were significantly greater in inflamed colon compared with controls. In control cells, pretreatment with 100 µM NaHS shifted the EC(50) for LEV-induced currents from 2838 (n = 6) to 154 (n = 8) nM. Sulfhydration of sulfonylurea receptor 2B (SUR2B) was induced by NaHS and colonic inflammation. These data suggest that sulfhydration of SUR2B induces allosteric modulation of K(ATP) currents in colonic inflammation.
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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.