RGD Reference Report - Transcription factor NF-kappa B is necessary for up-regulation of type 1 angiotensin II receptor mRNA in rat cardiac fibroblasts treated with tumor necrosis factor-alpha or interleukin-1 beta. - Rat Genome Database

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Transcription factor NF-kappa B is necessary for up-regulation of type 1 angiotensin II receptor mRNA in rat cardiac fibroblasts treated with tumor necrosis factor-alpha or interleukin-1 beta.

Authors: Cowling, RT  Gurantz, D  Peng, J  Dillmann, WH  Greenberg, BH 
Citation: Cowling RT, etal., J Biol Chem 2002 Feb 22;277(8):5719-24.
RGD ID: 70782
Pubmed: PMID:11600498   (View Abstract at PubMed)
DOI: DOI:10.1074/jbc.M107515200   (Journal Full-text)

Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta up-regulate type 1 angiotensin II receptor (AT(1)) mRNA and protein in cultured neonatal rat cardiac fibroblasts. The use of pharmacologic inhibitors and a degradation-resistant mutant I kappa B-alpha demonstrated that the transcription factor nuclear factor-kappa B (NF-kappa B) is necessary for cytokine-induced AT(1) up-regulation. The increase in AT(1) mRNA with TNF-alpha treatment is slow, reaching significance by 6-12 h and peaking by 24-48 h. Electrophoretic mobility shift assays revealed that NF-kappa B nuclear translocation was maintained for > or = 24 h with a single dose of TNF-alpha. Since prolonged NF-kappa B activation appeared necessary to maximize AT(1) up-regulation, the mechanism of persistent NF-kappa B activation was studied further. Stimulation with TNF-alpha induced a >10x increase in I kappa B kinase (IKK) activity that quickly diminished by 20 min. I kappa B-alpha and I kappa B-beta proteins were degraded during this time, and I kappa B-alpha was resynthesized subsequently by NF-kappa B-dependent transcription. However, I kappa B isoforms and IKK activity did not return completely to unstimulated values during a 12-h time course. These results suggest that low but persistent IKK activity and I kappa B degradation lead to prolonged NF-kappa B nuclear translocation and maximal AT(1) up-regulation in the continued presence of TNF-alpha.

Objects referenced in this article
Gene Agtr1b angiotensin II receptor, type 1b Rattus norvegicus

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