Key result
Angiotensin II induced Egr-1, increased fibronectin (fourfold, P<0.02) and laminin (twofold, P=0.05) mRNA levels, and decreased AT1-receptor mRNA levels (to 26%, P<0.001) in rat cardiac fibroblasts.
Why the study?
Does ANG II induce Egr-1 and matrix gene expression in cultured rat cardiac fibroblasts compared to other growth factors?
Population
Cultured rat cardiac fibroblasts
Comparison
Angiotensin II treatment (10-10 M) vs Other growth factors or basal/serum-free medium
Design
Preclinical
Follow-up
4-48 hours (in vitro)
Authors
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Ang II may promote fibroblast matrix remodeling; leaves open translation to human hypertrophy or therapy.
Does ANG II induce Egr-1 and matrix gene expression in cultured rat cardiac fibroblasts compared to other growth factors?
p-value: p=<0.02
ANG II plays a prominent and direct role in cardiac fibroblast changes associated with cardiac hypertrophy by inducing protooncogene expression and enhancing fibronectin mRNA levels via the AT1 receptor.
Iwami et al. (1996) studied Cardiac remodeling and ventricular hypertrophy. Angiotensin II (ANG II) vs. Basal/serum-free medium and other growth factors (EGF, NE, ET) was evaluated on Egr-1 and matrix gene expression (fibronectin, laminin) and AT1-receptor mRNA levels (p=<0.02). Angiotensin II induced Egr-1, increased fibronectin (fourfold, P<0.02) and laminin (twofold, P=0.05) mRNA levels, and decreased AT1-receptor mRNA levels (to 26%, P<0.001) in rat cardiac fibroblasts.
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