FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2737713057> ?p ?o ?g. }

• W2737713057 endingPage "1268.e11" @default.
• W2737713057 startingPage "1259" @default.
• W2737713057 abstract "BackgroundAllergic inflammation has long been implicated in asthmatic hyperresponsiveness of airway smooth muscle (ASM), but its underlying mechanism remains incompletely understood. Serving as G protein-coupled receptor agonists, several inflammatory mediators can induce membrane depolarization, contract ASM, and augment cholinergic contractile response. We hypothesized that the signal cascade integrating on membrane depolarization by the mediators might involve asthmatic hyperresponsiveness.ObjectiveWe sought to investigate the signaling transduction of inflammatory mediators in ASM contraction and assess its contribution in the genesis of hyperresponsiveness.MethodsWe assessed the capacity of inflammatory mediators to induce depolarization currents by electrophysiological analysis. We analyzed the phenotypes of transmembrane protein 16A (TMEM16A) knockout mice, applied pharmacological reagents, and measured the Ca2+ signal during ASM contraction. To study the role of the depolarization signaling in asthmatic hyperresponsiveness, we measured the synergistic contraction by methacholine and inflammatory mediators both ex vivo and in an ovalbumin-induced mouse model.ResultsInflammatory mediators, such as 5-hydroxytryptamin, histamine, U46619, and leukotriene D4, are capable of inducing Ca2+-activated Cl− currents in ASM cells, and these currents are mediated by TMEM16A. A combination of multiple analysis revealed that a G protein-coupled receptor–TMEM16A–voltage-dependent Ca2+ channel signaling axis was required for ASM contraction induced by inflammatory mediators. Block of TMEM16A activity may significantly inhibit the synergistic contraction of acetylcholine and the mediators and hence reduces hypersensitivity.ConclusionsA G protein-coupled receptor–TMEM16A–voltage-dependent Ca2+ channel axis contributes to inflammatory mediator-induced ASM contraction and synergistically activated TMEM16A by allergic inflammatory mediators with cholinergic stimuli. Allergic inflammation has long been implicated in asthmatic hyperresponsiveness of airway smooth muscle (ASM), but its underlying mechanism remains incompletely understood. Serving as G protein-coupled receptor agonists, several inflammatory mediators can induce membrane depolarization, contract ASM, and augment cholinergic contractile response. We hypothesized that the signal cascade integrating on membrane depolarization by the mediators might involve asthmatic hyperresponsiveness. We sought to investigate the signaling transduction of inflammatory mediators in ASM contraction and assess its contribution in the genesis of hyperresponsiveness. We assessed the capacity of inflammatory mediators to induce depolarization currents by electrophysiological analysis. We analyzed the phenotypes of transmembrane protein 16A (TMEM16A) knockout mice, applied pharmacological reagents, and measured the Ca2+ signal during ASM contraction. To study the role of the depolarization signaling in asthmatic hyperresponsiveness, we measured the synergistic contraction by methacholine and inflammatory mediators both ex vivo and in an ovalbumin-induced mouse model. Inflammatory mediators, such as 5-hydroxytryptamin, histamine, U46619, and leukotriene D4, are capable of inducing Ca2+-activated Cl− currents in ASM cells, and these currents are mediated by TMEM16A. A combination of multiple analysis revealed that a G protein-coupled receptor–TMEM16A–voltage-dependent Ca2+ channel signaling axis was required for ASM contraction induced by inflammatory mediators. Block of TMEM16A activity may significantly inhibit the synergistic contraction of acetylcholine and the mediators and hence reduces hypersensitivity. A G protein-coupled receptor–TMEM16A–voltage-dependent Ca2+ channel axis contributes to inflammatory mediator-induced ASM contraction and synergistically activated TMEM16A by allergic inflammatory mediators with cholinergic stimuli." @default.
• W2737713057 created "2017-07-31" @default.
• W2737713057 creator A5003635733 @default.
• W2737713057 creator A5007170702 @default.
• W2737713057 creator A5010025585 @default.
• W2737713057 creator A5011487190 @default.
• W2737713057 creator A5012395734 @default.
• W2737713057 creator A5017583651 @default.
• W2737713057 creator A5019736036 @default.
• W2737713057 creator A5020764523 @default.
• W2737713057 creator A5028354417 @default.
• W2737713057 creator A5032928959 @default.
• W2737713057 creator A5040317059 @default.
• W2737713057 creator A5044742215 @default.
• W2737713057 creator A5051368106 @default.
• W2737713057 creator A5052342599 @default.
• W2737713057 creator A5057816300 @default.
• W2737713057 creator A5062320569 @default.
• W2737713057 creator A5070964141 @default.
• W2737713057 creator A5071324604 @default.
• W2737713057 creator A5075401247 @default.
• W2737713057 creator A5083558362 @default.
• W2737713057 creator A5088563574 @default.
• W2737713057 creator A5091584882 @default.
• W2737713057 date "2018-04-01" @default.
• W2737713057 modified "2023-10-18" @default.
• W2737713057 title "Inflammatory mediators mediate airway smooth muscle contraction through a G protein-coupled receptor–transmembrane protein 16A–voltage-dependent Ca2+ channel axis and contribute to bronchial hyperresponsiveness in asthma" @default.
• W2737713057 cites W1974029350 @default.
• W2737713057 cites W1981005009 @default.
• W2737713057 cites W1981193117 @default.
• W2737713057 cites W1982946123 @default.
• W2737713057 cites W1987211770 @default.
• W2737713057 cites W1989470236 @default.
• W2737713057 cites W1994132777 @default.
• W2737713057 cites W2002423800 @default.
• W2737713057 cites W2002947342 @default.
• W2737713057 cites W2005402925 @default.
• W2737713057 cites W2007589345 @default.
• W2737713057 cites W2008839219 @default.
• W2737713057 cites W2009212458 @default.
• W2737713057 cites W2032921167 @default.
• W2737713057 cites W2036980397 @default.
• W2737713057 cites W2039252747 @default.
• W2737713057 cites W2046679315 @default.
• W2737713057 cites W2048575473 @default.
• W2737713057 cites W2049038183 @default.
• W2737713057 cites W2057989715 @default.
• W2737713057 cites W2060861289 @default.
• W2737713057 cites W2064943836 @default.
• W2737713057 cites W2065417952 @default.
• W2737713057 cites W2069238369 @default.
• W2737713057 cites W2076049916 @default.
• W2737713057 cites W2082147396 @default.
• W2737713057 cites W2101864423 @default.
• W2737713057 cites W2105569346 @default.
• W2737713057 cites W2117090406 @default.
• W2737713057 cites W2131075277 @default.
• W2737713057 cites W2136879864 @default.
• W2737713057 cites W2142388311 @default.
• W2737713057 cites W2143903809 @default.
• W2737713057 cites W2153668688 @default.
• W2737713057 cites W2155232620 @default.
• W2737713057 cites W2158893295 @default.
• W2737713057 cites W2162881883 @default.
• W2737713057 cites W2164789553 @default.
• W2737713057 cites W2338039769 @default.
• W2737713057 cites W2341680059 @default.
• W2737713057 cites W4255337810 @default.
• W2737713057 cites W2036354991 @default.
• W2737713057 doi "https://doi.org/10.1016/j.jaci.2017.05.053" @default.
• W2737713057 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28754608" @default.
• W2737713057 hasPublicationYear "2018" @default.
• W2737713057 type Work @default.
• W2737713057 sameAs 2737713057 @default.
• W2737713057 citedByCount "32" @default.
• W2737713057 countsByYear W27377130572018 @default.
• W2737713057 countsByYear W27377130572019 @default.
• W2737713057 countsByYear W27377130572020 @default.
• W2737713057 countsByYear W27377130572021 @default.
• W2737713057 countsByYear W27377130572022 @default.
• W2737713057 countsByYear W27377130572023 @default.
• W2737713057 crossrefType "journal-article" @default.
• W2737713057 hasAuthorship W2737713057A5003635733 @default.
• W2737713057 hasAuthorship W2737713057A5007170702 @default.
• W2737713057 hasAuthorship W2737713057A5010025585 @default.
• W2737713057 hasAuthorship W2737713057A5011487190 @default.
• W2737713057 hasAuthorship W2737713057A5012395734 @default.
• W2737713057 hasAuthorship W2737713057A5017583651 @default.
• W2737713057 hasAuthorship W2737713057A5019736036 @default.
• W2737713057 hasAuthorship W2737713057A5020764523 @default.
• W2737713057 hasAuthorship W2737713057A5028354417 @default.
• W2737713057 hasAuthorship W2737713057A5032928959 @default.
• W2737713057 hasAuthorship W2737713057A5040317059 @default.
• W2737713057 hasAuthorship W2737713057A5044742215 @default.
• W2737713057 hasAuthorship W2737713057A5051368106 @default.
• W2737713057 hasAuthorship W2737713057A5052342599 @default.
• W2737713057 hasAuthorship W2737713057A5057816300 @default.
• W2737713057 hasAuthorship W2737713057A5062320569 @default.

• next