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DC Field | Value | Language |
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dc.citation.endPage | 8710 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 8701 | - |
dc.citation.title | JOURNAL OF CELLULAR PHYSIOLOGY | - |
dc.citation.volume | 233 | - |
dc.contributor.author | Hwang, Hyeon-Jeong | - |
dc.contributor.author | Park, Kyoung-Su | - |
dc.contributor.author | Choi, Jang Hyun | - |
dc.contributor.author | Cocco, Lucio | - |
dc.contributor.author | Jang, Hyun-Jun | - |
dc.contributor.author | Suh, Pann-Ghill | - |
dc.date.accessioned | 2023-12-21T20:44:05Z | - |
dc.date.available | 2023-12-21T20:44:05Z | - |
dc.date.created | 2018-07-03 | - |
dc.date.issued | 2018-05 | - |
dc.description.abstract | The zafirlukast has been reported to be anti-inflammatory and widely used to alleviate the symptoms of asthma. However, its influence on insulin secretion in pancreatic -cells has not been investigated. Herein, we examined the effects of zafirlukast on insulin secretion and the potential underlying mechanisms. Among the cysteinyl leukotriene receptor 1 antagonists, zafirlukast, pranlukast, and montelukast, only zafirlukast enhanced insulin secretion in a concentration-dependent manner in both low and high glucose conditions and elevated the level of [Ca2+](i), further activating Ca2+/calmodulin-dependent protein kinase II (CaMKII), protein kinase B (AKT), and extracellular signal-regulated kinase (ERK) signaling. These effects were nearly abolished by the L-type Ca2+ channel antagonist nifedipine, while treatment with thapsigargin, a sarco/endoplasmic reticulum Ca2+ ATPase inhibitor, did not have the same effect, suggesting that zafirlukast primarily induces the entry of extracellular Ca2+ rather than intracellular Ca2+ from the endoplasmic reticulum. Zafirlukast treatment resulting in a significant drop in glucose levels and increased insulin secretion in C57BL/6J mice. These findings will contribute to an improved understanding of the side effects of zafirlukast and potential candidate for a therapeutic intervention in diabetes. | - |
dc.identifier.bibliographicCitation | JOURNAL OF CELLULAR PHYSIOLOGY, v.233, no.11, pp.8701 - 8710 | - |
dc.identifier.doi | 10.1002/jcp.26750 | - |
dc.identifier.issn | 0021-9541 | - |
dc.identifier.scopusid | 2-s2.0-85054100110 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/24265 | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/abs/10.1002/jcp.26750 | - |
dc.identifier.wosid | 000446264900029 | - |
dc.language | 영어 | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.title | Zafirlukast promotes insulin secretion by increasing calcium influx through L-type calcium channels | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Cell Biology; Physiology | - |
dc.relation.journalResearchArea | Cell Biology; Physiology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | hypoglycemia | - |
dc.subject.keywordAuthor | insulin secretion | - |
dc.subject.keywordAuthor | intracellular calcium | - |
dc.subject.keywordAuthor | L-type calcium channels | - |
dc.subject.keywordAuthor | zafirlukast | - |
dc.subject.keywordPlus | PANCREATIC BETA-CELLS | - |
dc.subject.keywordPlus | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | - |
dc.subject.keywordPlus | LEUKOTRIENE RECEPTOR ANTAGONISTS | - |
dc.subject.keywordPlus | REGULATED KINASES | - |
dc.subject.keywordPlus | PROTEIN-KINASES | - |
dc.subject.keywordPlus | GLUCOSE | - |
dc.subject.keywordPlus | ASTHMA | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
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