Key result
Angiotensin II induced accumulation of Egr-1 mRNA and protein in rat vascular smooth muscle cells, an effect that was blocked by the Ang II receptor antagonist EXP3174.
Why the study?
Does EXP3174 block Angiotensin II-induced Egr-1 expression in rat vascular smooth muscle cells?
Does EXP3174 block Angiotensin II-induced Egr-1 expression in rat vascular smooth muscle cells?
Angiotensin II induces Egr-1 expression in rat vascular smooth muscle cells via the PI signaling system, an effect that is blocked by the receptor antagonist EXP3174.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications from rat cells; leaves open Egr-1 role in human vascular disease.
The effect of angiotensin II (Ang II) on the early growth response gene-1 (Egr-1) mRNA, on the Egr-1 protein and on the phosphoinositide PI turnover signalling system was investigated in the presence and absence of EXP3174, a potent non-peptide Ang II receptor antagonist. Ang II induced an accumulation of 3.4 kb Egr-1 mRNA and the 80 kDa Egr-1 protein, with a maximum at 30 min and 60 min, respectively. EXP3174 blocked the Ang II-induced increase of inositol phosphates, Egr-1 mRNA and the Egr-1 protein, suggesting the involvement of the PI signalling system by the expression of the Egr-1 gene.
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Sachinidis et al. (1992) studied this question. Angiotensin II and EXP3174 vs. Absence of EXP3174 was evaluated on Egr-1 mRNA and protein accumulation. Angiotensin II induced accumulation of Egr-1 mRNA and protein in rat vascular smooth muscle cells, an effect that was blocked by the Ang II receptor antagonist EXP3174.
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