Angiotensin II represses Npr1 expression and receptor function by recruitment of transcription factors CREB and HSF-4a and activation of HDACs.

Scientific Reports
Kiran K AriseKailash N Pandey

Abstract

The two vasoactive hormones, angiotensin II (ANG II; vasoconstrictive) and atrial natriuretic peptide (ANP; vasodilatory) antagonize the biological actions of each other. ANP acting through natriuretic peptide receptor-A (NPRA) lowers blood pressure and blood volume. We tested hypothesis that ANG II plays critical roles in the transcriptional repression of Npr1 (encoding NPRA) and receptor function. ANG II significantly decreased NPRA mRNA and protein levels and cGMP accumulation in cultured mesangial cells and attenuated ANP-mediated relaxation of aortic rings ex vivo. The transcription factors, cAMP-response element-binding protein (CREB) and heat-shock factor-4a (HSF-4a) facilitated the ANG II-mediated repressive effects on Npr1 transcription. Tyrosine kinase (TK) inhibitor, genistein and phosphatidylinositol 3-kinase (PI-3K) inhibitor, wortmannin reversed the ANG II-dependent repression of Npr1 transcription and receptor function. ANG II enhanced the activities of Class I histone deacetylases (HDACs 1/2), thereby decreased histone acetylation of H3K9/14ac and H4K8ac. The repressive effect of ANG II on Npr1 transcription and receptor signaling seems to be transduced by TK and PI-3K pathways and modulated by CREB, HSF-4a, HDA...Continue Reading

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Citations

Sep 11, 2020·Arteriosclerosis, Thrombosis, and Vascular Biology·Moritz Lindquist LiljeqvistJoy Roy
Mar 31, 2021·Molecular and Cellular Endocrinology·Fitra RiantoMatthew A Sparks

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Methods Mentioned

BETA
transfection
electrophoretic mobility shift assay
electrophoresis
acetylation
gel mobility shift
histone acetylation
enzyme-linked immunosorbent assay
PCR
FCS
X-ray

Software Mentioned

GraphPad prism
AlphaView

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