RGD Reference Report - Differential expression of cytokines in the rat heart in response to sustained volume overload. - Rat Genome Database

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Differential expression of cytokines in the rat heart in response to sustained volume overload.

Authors: Dai, RP  Dheen, ST  He, BP  Tay, SS 
Citation: Dai RP, etal., Eur J Heart Fail. 2004 Oct;6(6):693-703.
RGD ID: 1581939
Pubmed: PMID:15542404   (View Abstract at PubMed)
DOI: DOI:10.1016/j.ejheart.2003.11.014   (Journal Full-text)

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)-alpha, interleukin (IL)-1beta, interleukin (IL)-6 and transforming growth factor (TGF)-beta(1). 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-1beta and IL-6 gene and protein levels were upregulated throughout the time of measurement. Immunohistochemistry demonstrated that IL-1beta 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-1beta immunoreactive cells were mainly localized in the blood vessels whereas the IL-6 positive cells were composed of non-myocytes and cardiomyocytes. TGF-beta(1) 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-1beta and IL-6 in response to volume overload, TNF-alpha 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-alpha, IL-1beta and IL-6 suggest that the induction of IL-6 and IL-1beta is independent of TNF-alpha mediated pathways in this animal model.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Cardiomegaly  ISOIl1b (Rattus norvegicus)1581939; 1581939mRNA and protein:increased expression:heartRGD 
Cardiomegaly  ISOIl6 (Rattus norvegicus)1581939; 1581939mRNA and protein:increased expression:heartRGD 
Cardiomegaly  IEP 1581939; 1581939; 1581939mRNA and protein:increased expression:heartRGD 
Cardiomegaly  ISOTgfb1 (Rattus norvegicus)1581939; 1581939mRNA and protein:increased expression:heartRGD 

Objects Annotated

Genes (Rattus norvegicus)
Il1b  (interleukin 1 beta)
Il6  (interleukin 6)
Tgfb1  (transforming growth factor, beta 1)

Genes (Mus musculus)
Il1b  (interleukin 1 beta)
Il6  (interleukin 6)
Tgfb1  (transforming growth factor, beta 1)

Genes (Homo sapiens)
IL1B  (interleukin 1 beta)
IL6  (interleukin 6)
TGFB1  (transforming growth factor beta 1)

Objects referenced in this article
Gene LTA lymphotoxin alpha Homo sapiens
Gene Lta lymphotoxin A Mus musculus
Gene Lta lymphotoxin alpha Rattus norvegicus

Additional Information