Please use this identifier to cite or link to this item:
|Title:||Differential expression of cytokines in the rat heart in response to sustained volume overload||Authors:||Dai, R.P.
|Issue Date:||2004||Citation:||Dai, R.P., Dheen, S.T., He, B.P., Tay, S.S.W. (2004). Differential expression of cytokines in the rat heart in response to sustained volume overload. European Journal of Heart Failure 6 (6) : 693-703. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ejheart.2003.11.014||Abstract:||Objective: The present study aimed to investigate whether sustained volume overload is capable of inducing persistent upregulation of cardiac cytokines including tumor necrosis factor alpha (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6 and transforming growth factor (TGF)-β1. Methods and Results: Volume overload-induced heart hypertrophy in rats was established by aortacaval fistula, and the cardiac cytokines were measured in the myocardium from 1 to 4 weeks after operation. In the post-fistula rats, cardiac IL-1β and IL-6 gene and protein levels were upregulated throughout the time of measurement. Immunohistochemistry demonstrated that IL-1β and IL-6 immunoreactive cells were widely distributed in the myocardium in the earlier time intervals, and mainly localized in the regions close to the endocardium in the later time intervals. The cardiac IL-1β immunoreactive cells were mainly localized in the blood vessels whereas the IL-6 positive cells were composed of non-myocytes and cardiomyocytes. TGF-β1 positive staining was increased in the myocardium up to 3 weeks after aortacaval fistula and then decreased to basal levels thereafter. In contrast to the activation of cardiac IL-1β and IL-6 in response to volume overload, TNF-α expression appeared unaltered in response to sustained volume overload in the transcription and protein levels. Conclusion: The results of the present study indicate that sustained volume overload is capable of inducing persistent upregulation of some cardiac cytokines. In addition, the differential expressions of TNF-α, IL-1β and IL-6 suggest that the induction of IL-6 and IL-1β is independent of TNF-α mediated pathways in this animal model. © 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.||Source Title:||European Journal of Heart Failure||URI:||http://scholarbank.nus.edu.sg/handle/10635/33560||ISSN:||13889842||DOI:||10.1016/j.ejheart.2003.11.014|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Jan 22, 2020
WEB OF SCIENCETM
checked on Jan 22, 2020
checked on Jan 29, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.