Carbon monoxide activates large-conductance calcium-activated potassium channels of human cardiac fibroblasts through various mechanisms
DC Field | Value | Language |
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dc.contributor.author | Bae, Hyemi | - |
dc.contributor.author | Kim, Taeho | - |
dc.contributor.author | Lim, Inja | - |
dc.date.accessioned | 2021-10-26T05:40:14Z | - |
dc.date.available | 2021-10-26T05:40:14Z | - |
dc.date.issued | 2021-05 | - |
dc.identifier.issn | 1226-4512 | - |
dc.identifier.issn | 2093-3827 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/50705 | - |
dc.description.abstract | Carbon monoxide (CO) is a cardioprotectant and potential cardiovascular therapeutic agent. Human cardiac fibroblasts (HCFs) are important determinants of myocardial structure and function. Large-conductance Ca2+-activated K+ (BK) channel is a potential therapeutic target for cardiovascular disease. We investigated whether CO modulates BK channels and the signaling pathways in HCFs using whole-cell mode patch-clamp recordings. CO-releasing molecules (CORMs; CORM-2 and CORM-3) significantly increased the amplitudes of BK currents (IBK). The CO-induced stimulating effects on IBK were blocked by pre-treatment with specific nitric oxide synthase (NOS) blockers (L-N-G-monomethyl arginine citrate and L-N-G-nitroarginine methyl ester). 8-bromo-cyclic GMP increased IBK. KT5823 (inhibits PKG) or ODQ (inhibits soluble guanylate cyclase) blocked the CO-stimulating effect on IBK. Moreover, 8-bromo-cyclic AMP also increased IBK, and pre-treatment with KT5720 (inhibits PKA) or SQ22536 (inhibits adenylate cyclase) blocked the CO effect. Pre-treatment with N-ethylmaleimide (a thiol-alkylating reagent) also blocked the CO effect on IBK, and DL-dithiothreitol (a reducing agent) reversed the CO effect. These data suggest that CO activates IBK through NO via the NOS and through the PKG, PKA, and S-nitrosylation pathways. | - |
dc.format.extent | 11 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY | - |
dc.title | Carbon monoxide activates large-conductance calcium-activated potassium channels of human cardiac fibroblasts through various mechanisms | - |
dc.type | Article | - |
dc.identifier.doi | 10.4196/kjpp.2021.25.3.227 | - |
dc.identifier.bibliographicCitation | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.25, no.3, pp 227 - 237 | - |
dc.identifier.kciid | ART002712645 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000641146000006 | - |
dc.identifier.scopusid | 2-s2.0-85105304518 | - |
dc.citation.endPage | 237 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 227 | - |
dc.citation.title | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY | - |
dc.citation.volume | 25 | - |
dc.type.docType | Article | - |
dc.publisher.location | 대한민국 | - |
dc.subject.keywordAuthor | Calcium-activated potassium channel | - |
dc.subject.keywordAuthor | Carbon monoxide | - |
dc.subject.keywordAuthor | Nitric oxide | - |
dc.subject.keywordAuthor | Protein kinases | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
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