ArticleThe Journal of biological chemistry2010
Lipopolysaccharides up-regulate Kir6.1/SUR2B channel expression and enhance vascular KATP channel activity via NF-kappaB-dependent signaling.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Characterization of four structurally diverse inhibitors of SUR2-containing KChannels (Austin, Tex.) · 2024Article
- Circadian Control of the Response of Macrophages to Plasmodium Spp.-Infected Red Blood Cells.ImmunoHorizons · 2024Article
- Discovery and Characterization of VU0542270, the First Selective Inhibitor of Vascular Kir6.1/SUR2B KMolecular pharmacology · 2024Article
- Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022Review
- ATP-Sensitive Potassium Channels in Migraine: Translational Findings and Therapeutic Potential.Cells · 2022Review
- Effect of visfatin on KAging · 2022Article
- Role of ATP-sensitive potassium channels on hypoxic pulmonary vasoconstriction in endotoxemia.Respiratory research · 2018Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- A Protective Role of Glibenclamide in Inflammation-Associated Injury.Mediators of inflammation · 2017Review
- Sarcolemmal ATP-sensitive potassium channel protects cardiac myocytes against lipopolysaccharide-induced apoptosis.International journal of molecular medicine · 2016Article
- Sensitivity of KATP channels to cellular metabolic disorders and the underlying structural basis.Acta pharmacologica Sinica · 2016Article
- Optogenetic approach for functional assays of the cardiovascular system by light activation of the vascular smooth muscle.Vascular pharmacology · 2015Article
- Endotoxemia-mediated inflammation potentiates aminoglycoside-induced ototoxicity.Science translational medicine · 2015Article
- Effects of pinacidil on changes to the microenvironment around the incision site, of a skin/muscle incision and retraction, in a rat model of postoperative pain.Molecular medicine reports · 2015Article
- Interception of the endotoxin-induced arterial hyporeactivity to vasoconstrictors.Vascular pharmacology · 2014Article
- S-glutathionylation of ion channels: insights into the regulation of channel functions, thiol modification crosstalk, and mechanosensing.Antioxidants & redox signaling · 2014Review
- The role of ATP-sensitive potassium channels in cellular function and protection in the cardiovascular system.British journal of pharmacology · 2014Review
- Differential sensitivities of the vascular K(ATP) channel to various PPAR activators.Biochemical pharmacology · 2013Article
- Prolonged exposure to methylglyoxal causes disruption of vascular KATP channel by mRNA instability.American journal of physiology. Cell physiology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Sepsis is a severe medical condition causing a large number of deaths worldwide. Recent studies indicate that the septic susceptibility is attributable to the vascular ATP-sensitive K(+) (K(ATP)) channel. However, the mechanisms underlying the channel modulation in sepsis are still unclear. Here we show evidence for the modulation of vascular K(ATP) channel by septic pathogen lipopolysaccharides (LPS). In isolated mesenteric arterial rings, phenylephrine (PE) produced concentration-dependent vasoconstriction that was relaxed by pinacidil, a selective K(ATP) channel opener. The PE response was disrupted with a LPS treatment. In acutely dissociated aortic smooth myocytes the LPS treatment augmented K(ATP) channel activity, and hyperpolarized the cells. Quantitative PCR analysis showed that LPS raised Kir6.1 and SUR2B transcripts in a concentration-dependent manner, which was suppressed by transcriptional inhibition. Consistently, the same LPS treatment did not affect Kir6.1/SUR2B channels in a heterologous expression system. The LPS effect on Kir6.1 and SUR2B expression was abolished in the presence of NF-kappaB inhibitors. Several other Toll-like receptor ligands also stimulated Kir6.1 and SUR2B expression to a similar degree as LPS. Thus, the effect of LPS on vasodilation involves up-regulation of K(ATP) channel expression, in which the NF-kappaB-dependent signaling plays an important role.
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Registered trials
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.