Cited 80 times in
Protease-activated receptor 2 exerts local protection and mediates some systemic complications in acute pancreatitis
DC Field | Value | Language |
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dc.contributor.author | 김경환 | - |
dc.contributor.author | 이민구 | - |
dc.contributor.author | 조경희 | - |
dc.date.accessioned | 2015-07-14T16:46:57Z | - |
dc.date.available | 2015-07-14T16:46:57Z | - |
dc.date.issued | 2004 | - |
dc.identifier.issn | 0016-5085 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/111578 | - |
dc.description.abstract | BACKGROUND & AIMS: Protease-activated receptor 2 can be stimulated by interstitially released trypsin during acute inflammation of the pancreas. In this study, we investigated the roles of pancreatic and circulatory protease-activated receptor 2 in the pathogenesis of acute pancreatitis by using in vitro and in vivo model systems. METHODS: Physiological and pathologic effects of protease-activated receptor 2 activation were measured in isolated pancreatic cells and in rats with experimental pancreatitis. Consequences of protease-activated receptor 2 activation on the systemic and inflammatory responses were measured after treatments with trypsin or protease-activated receptor 2-activating peptide. RESULTS: Stimulation of protease-activated receptor 2 in rat pancreatic acinar cells activated short-lasting (Ca(2+) signaling) and long-lasting (extracellular signal-related kinase) signaling pathways and protected the cells against bile-induced cell damage. More importantly, protease-activated receptor 2 activation ameliorated the pathologic effects observed in the in vivo model of cerulein-induced pancreatitis. Trypsin in the circulation of rats with taurocholate-induced severe acute pancreatitis reached levels sufficient to activate endothelial and immune cells to stimulate nitric oxide and interleukin-8 production, respectively. Most notably, activation of systemic protease-activated receptor 2 by circulating protease-activated receptor 2 agonists induced a hemodynamic response pattern similar to that observed in rats with severe acute pancreatitis. The effects of protease-activated receptor 2 agonists and acute pancreatitis were not additive. CONCLUSIONS: These findings suggest that protease-activated receptor 2 may have a dual role in acute pancreatitis: protecting acinar and duct cells against pancreatitis-induced cell damage while mediating or aggravating the systemic complications of acute pancreatitis, which are the major cause of mortality in the early phase of necrotizing pancreatitis. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1844~1859 | - |
dc.relation.isPartOf | GASTROENTEROLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Acute Disease | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Blood Pressure | - |
dc.subject.MESH | Cell Survival/physiology | - |
dc.subject.MESH | Cells, Cultured | - |
dc.subject.MESH | Ceruletide | - |
dc.subject.MESH | Endopeptidases/pharmacology | - |
dc.subject.MESH | Gene Expression | - |
dc.subject.MESH | In Vitro Techniques | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Monocytes/pathology | - |
dc.subject.MESH | Pancreas/cytology | - |
dc.subject.MESH | Pancreatic Ducts/cytology | - |
dc.subject.MESH | Pancreatitis/chemically induced | - |
dc.subject.MESH | Pancreatitis/metabolism* | - |
dc.subject.MESH | Pancreatitis/pathology* | - |
dc.subject.MESH | Rats | - |
dc.subject.MESH | Rats, Sprague-Dawley | - |
dc.subject.MESH | Receptor, PAR-2/genetics* | - |
dc.subject.MESH | Receptor, PAR-2/metabolism* | - |
dc.subject.MESH | Trypsin/blood | - |
dc.title | Protease-activated receptor 2 exerts local protection and mediates some systemic complications in acute pancreatitis | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Family Medicine (가정의학) | - |
dc.contributor.googleauthor | Wan Namkung | - |
dc.contributor.googleauthor | Wonsun Han | - |
dc.contributor.googleauthor | Min Goo Lee | - |
dc.contributor.googleauthor | Kyung Hwan Kim | - |
dc.contributor.googleauthor | Kyung Hee Cho | - |
dc.contributor.googleauthor | Shmuel Muallem | - |
dc.contributor.googleauthor | Xiang Luo | - |
dc.identifier.doi | 10.1053/j.gastro.2004.03.019 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.relation.journalcode | J00917 | - |
dc.identifier.eissn | 1528-0012 | - |
dc.identifier.pmid | 15188179 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0016508504004494 | - |
dc.contributor.alternativeName | Kim, Kyung Hwan | - |
dc.contributor.alternativeName | Lee, Min Goo | - |
dc.contributor.alternativeName | Cho, Kyung Hee | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 126 | - |
dc.citation.number | 7 | - |
dc.citation.startPage | 1844 | - |
dc.citation.endPage | 1859 | - |
dc.identifier.bibliographicCitation | GASTROENTEROLOGY, Vol.126(7) : 1844-1859, 2004 | - |
dc.identifier.rimsid | 34931 | - |
dc.type.rims | ART | - |
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