title: Induction of cytokine expression in rat post-ischemic sinoatrial node (SAN).
abstract: The aim of this study was to determine the spatial and temporal expression of various pro-inflammatory cytokines in the peri-sinoatrial nodal area after atrial infarction. Rats were subjected to permanent atrial infarction, in particular, sinoatrial node (SAN) infarction and sacrificed at various time points up to 7 days. Real-time polymerase chain reaction analysis demonstrated that mRNA levels of tumor necrosis factor alpha (TNF-alpha), interleukin-1beta, interleukin-6, and transforming growth factor beta 1 (TGF-beta(1)) were upregulated in the peri-sinoatrial nodal area after atrial infarction. Immunostaining for TNF-alpha and TGF-beta(1) proteins revealed that both cytokines were expressed persistently up to 7 days after atrial infarction around the peri-sinoatrial nodal area. Furthermore, the infiltrating inflammatory cells immunoreactive for both cytokines were predominant within the infarct SAN. In situ hybridization analysis showed that TNF-alpha gene expression was enhanced in the inflammatory cells and myocardium within the peri-sinoatrial nodal area in response to the infarction. These results provide evidence for the local expression of cytokines in the post-ischemic peri-sinoatrial nodal area, suggesting that the upregulation of the cytokines might be associated with the atrial arrhythmia observed after acute myocardial infarction.
authors.affiliation: Department of Anatomy, Faculty of Medicine, National University of Singapore, Lower Kent Ridge Road, Singapore 117597.
authors.forename: R P
authors.initials: RP
authors.lastname: Dai
authors.forename: S Thameem
authors.initials: ST
authors.lastname: Dheen
authors.forename: S S W
authors.initials: SS
authors.lastname: Tay
mesh_terms: D000818:Animals; D001146:Arrhythmia, Sinus / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D016207:Cytokines / Q000235:genetics* / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression / Q000502:physiology; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D017202:Myocardial Ischemia / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012849:Sinoatrial Node / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D012333:RNA, Messenger; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha