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Article: Mast cell contributes to cardiomyocyte apoptosis after coronary microembolization

TitleMast cell contributes to cardiomyocyte apoptosis after coronary microembolization
Authors
Issue Date2006
PublisherHistochemical Society. The Journal's web site is located at http://intl.jhc.org
Citation
Journal Of Histochemistry And Cytochemistry, 2006, v. 54 n. 5, p. 515-523 How to Cite?
AbstractCoronary microembolization (CME) is associated with progressive myocardial dysfunction despite restoration of coronary flow reserve (CFR). The potential pathophysiological role of mast cells (MCs) remains unclear. Therefore, we induced CME in 18 miniswines and determined whether MC accumulation occurs and their effects on local cytokine secretion [interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α)]; cardiomyocyte apoptosis; and collagen formation at day 1 (D1), day 7 (D7), and day 30 (D30) after CME. Four sham-operated animals without CME (controls) and six animals treated with a MC stabilization agent (tranilast) for 30 days after CME were also studied. CFR decreased at D1 but returned to baseline level at D7 and D30. Coronary sinus levels of IL-6, IL-8, and TNF-α increased significantly at D1 and D7 (p<0.01 vs baseline). Levels of IL-6 and IL-8 at D30 returned to baseline level, but not those of TNF-α. The numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and collagen volume fraction (CVF) over CME myocardium at D1, D7, and D30 were significantly higher than controls (p<0.01). Treatment with tranilast significantly reduced the serum level of TNF-α, numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and CVF at D30 (all p<0.05). There was a significant positive correlation between the numbers of MCs with % apoptotic cardiomyocytes (r = 0.77, p<0.001) and CVF (r = 0.75, p<0.001) over the CME myocardium. Despite restoration of CFR, cardiomyocyte apoptosis persisted after CME and was positively correlated with the number of MCs but was prevented with tranilast treatment. These findings suggest that MCs contribute to cardiomyocyte apoptosis after CME. © The Histochemical Society, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/162967
ISSN
2015 Impact Factor: 1.953
2015 SCImago Journal Rankings: 1.187
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, QYen_US
dc.contributor.authorGe, JBen_US
dc.contributor.authorChen, JZen_US
dc.contributor.authorZhu, JHen_US
dc.contributor.authorZhang, LHen_US
dc.contributor.authorLau, CPen_US
dc.contributor.authorTse, HFen_US
dc.date.accessioned2012-09-05T05:25:58Z-
dc.date.available2012-09-05T05:25:58Z-
dc.date.issued2006en_US
dc.identifier.citationJournal Of Histochemistry And Cytochemistry, 2006, v. 54 n. 5, p. 515-523en_US
dc.identifier.issn0022-1554en_US
dc.identifier.urihttp://hdl.handle.net/10722/162967-
dc.description.abstractCoronary microembolization (CME) is associated with progressive myocardial dysfunction despite restoration of coronary flow reserve (CFR). The potential pathophysiological role of mast cells (MCs) remains unclear. Therefore, we induced CME in 18 miniswines and determined whether MC accumulation occurs and their effects on local cytokine secretion [interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α)]; cardiomyocyte apoptosis; and collagen formation at day 1 (D1), day 7 (D7), and day 30 (D30) after CME. Four sham-operated animals without CME (controls) and six animals treated with a MC stabilization agent (tranilast) for 30 days after CME were also studied. CFR decreased at D1 but returned to baseline level at D7 and D30. Coronary sinus levels of IL-6, IL-8, and TNF-α increased significantly at D1 and D7 (p<0.01 vs baseline). Levels of IL-6 and IL-8 at D30 returned to baseline level, but not those of TNF-α. The numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and collagen volume fraction (CVF) over CME myocardium at D1, D7, and D30 were significantly higher than controls (p<0.01). Treatment with tranilast significantly reduced the serum level of TNF-α, numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and CVF at D30 (all p<0.05). There was a significant positive correlation between the numbers of MCs with % apoptotic cardiomyocytes (r = 0.77, p<0.001) and CVF (r = 0.75, p<0.001) over the CME myocardium. Despite restoration of CFR, cardiomyocyte apoptosis persisted after CME and was positively correlated with the number of MCs but was prevented with tranilast treatment. These findings suggest that MCs contribute to cardiomyocyte apoptosis after CME. © The Histochemical Society, Inc.en_US
dc.languageengen_US
dc.publisherHistochemical Society. The Journal's web site is located at http://intl.jhc.orgen_US
dc.relation.ispartofJournal of Histochemistry and Cytochemistryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnthranilic Acids - Pharmacologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCollagen - Metabolismen_US
dc.subject.meshCoronary Circulationen_US
dc.subject.meshCoronary Vessels - Pathology - Physiopathologyen_US
dc.subject.meshEmbolism - Pathology - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshInterleukin-6 - Metabolismen_US
dc.subject.meshInterleukin-8 - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMast Cells - Drug Effects - Physiologyen_US
dc.subject.meshMicroscopy, Electron, Transmissionen_US
dc.subject.meshMyocardium - Metabolism - Pathology - Ultrastructureen_US
dc.subject.meshMyocytes, Cardiac - Physiologyen_US
dc.subject.meshSwineen_US
dc.subject.meshSwine, Miniatureen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolismen_US
dc.titleMast cell contributes to cardiomyocyte apoptosis after coronary microembolizationen_US
dc.typeArticleen_US
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1369/jhc.5A6804.2005en_US
dc.identifier.pmid16344327-
dc.identifier.scopuseid_2-s2.0-33646036134en_US
dc.identifier.hkuros114956-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646036134&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume54en_US
dc.identifier.issue5en_US
dc.identifier.spage515en_US
dc.identifier.epage523en_US
dc.identifier.isiWOS:000237101200003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhang, QY=35331268500en_US
dc.identifier.scopusauthoridGe, JB=7202197226en_US
dc.identifier.scopusauthoridChen, JZ=36107692700en_US
dc.identifier.scopusauthoridZhu, JH=7405692054en_US
dc.identifier.scopusauthoridZhang, LH=12761577500en_US
dc.identifier.scopusauthoridLau, CP=7401968501en_US
dc.identifier.scopusauthoridTse, HF=7006070805en_US

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