RGD Reference Report - Changes in cardiac structure in hypertension produced by placental ischemia in pregnant rats: effect of tumor necrosis factor blockade. - Rat Genome Database

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Changes in cardiac structure in hypertension produced by placental ischemia in pregnant rats: effect of tumor necrosis factor blockade.

Authors: Gutkowska, J  Granger, JP  Lamarca, BB  Danalache, BA  Wang, D  Jankowski, M 
Citation: Gutkowska J, etal., J Hypertens. 2011 Apr 17.
RGD ID: 5131211
Pubmed: PMID:21505354   (View Abstract at PubMed)
DOI: DOI:10.1097/HJH.0b013e3283468392   (Journal Full-text)

OBJECTIVES: Chronic reduction of uteroplacental perfusion pressure (RUPP) in pregnant rats leads to placental ischemia, maternal endothelial cell dysfunction, hypertension and elevated levels of tumor necrosis factor-alpha (TNF-alpha). In this study we investigated the hypothesis that placental ischemia in pregnant rat, a model of preeclampsia, stimulates cardiac hypertrophy and fibrosis via a TNF-alpha-dependent mechanism. METHODS: Normal pregnant Sprague-Dawley rats and RUPP rats were evaluated on day 19 of gestation. To test the role of TNF-alpha in mediating change in the RUPP rat heart, a TNF-alpha inhibitor, etanercept, was administered on day 18 of gestation at a dose of 0.8 mg/kg, s.c. RESULTS: In comparison to normal pregnant rats, RUPP animals display enlarged cardiomyocytes, microvascular rarefaction, fibrosis, apoptosis as well as increased expression of markers of heart hypertrophy and fibrosis. Etanercept (E) treatment prevented enlargement of cardiomyocytes, fibrosis and apoptosis and this was accompanied by significantly lowered blood pressure in RUPP rats. Etanercept treatment lowered expression of mRNA for brain natriuretic peptide, a marker of cardiac hypertrophy. It also heightened expression of endothelial nitric oxide synthase and its phosphorylation as well as oxytocin receptor identified in cardiac microvessels. TNF-alpha inhibition prevented microvascular rarefaction in the heart as indicated by augmented CD31, a marker of angiogenesis. CONCLUSIONS: These results suggest that RUPP leads to microvascular rarefaction in the heart, exaggerated cardiomyocyte size, apoptosis, fibrosis, and the alteration of cardiac gene expression that are modulated by the inflammatory cytokine TNFalpha.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TNFRSF1BHumanpre-eclampsia  IDA human protein in rat modelRGD 
Tnfrsf1bRatpre-eclampsia  ISOTNFRSF1B (Homo sapiens)human protein in rat modelRGD 
Tnfrsf1bMousepre-eclampsia  ISOTNFRSF1B (Homo sapiens)human protein in rat modelRGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnfrsf1b  (TNF receptor superfamily member 1B)

Genes (Mus musculus)
Tnfrsf1b  (tumor necrosis factor receptor superfamily, member 1b)

Genes (Homo sapiens)
TNFRSF1B  (TNF receptor superfamily member 1B)


Additional Information