scholarly journals Retinoic acid‐induced regulation of guanylyl cyclase/natriuretic peptide receptor‐A gene expression in gene‐targeted mice via histone H3 modifications

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Prerna Kumar ◽  
Ramu Periyasamy ◽  
Subhankar Das ◽  
Kailash N Pandey
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Histone H3 ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A

Angiotensin II Represses Guanylyl Cyclase/Natriuretic Peptide Receptor‐A Gene Expression and Receptor Signaling and Function

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Kiran K. Arise ◽  
Prerna Kumar ◽  
Ramachandran Samivel ◽  
Hanqing Zhao ◽  
Sarah Lindsey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Natriuretic Peptide Receptor ◽  
Receptor Signaling ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A ◽  
And Function

Genetic disruption of guanylyl cyclase/natriuretic peptide receptor-A upregulates ACE and AT1 receptor gene expression and signaling: role in cardiac hypertrophy

2007 ◽  
Vol 31 (2) ◽  
pp. 193-202 ◽  
Author(s):  
Elangovan Vellaichamy ◽  
Di Zhao ◽  
Naveen Somanna ◽  
Kailash N. Pandey
Keyword(s):  
Gene Expression ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Heart Weight ◽  
Natriuretic Peptide Receptor ◽  
Wild Type ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A ◽  
Npr1 Gene

Guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) signaling antagonizes the physiological effects mediated by the renin-angiotensin system (RAS). The objective of this study was to determine whether the targeted-disruption of Npr1 gene (coding for GC-A/NPRA) leads to the activation of cardiac RAS genes involved on the hypertrophic remodeling process. The Npr1 gene-knockout ( Npr1 −/−) mice showed 30–35 mmHg higher systolic blood pressure (SBP) and a 63% greater heart weight-to-body weight (HW/BW) ratio compared with wild-type ( Npr1 +/+) mice. The mRNA levels of both angiotensin-converting enzyme and angiotensin II type 1a receptor were increased by three- and fourfold, respectively, in Npr1 −/− null mutant mice hearts compared with the wild-type Npr1 +/+ mice hearts. In parallel, the expression levels of interleukin-6 and tumor necrosis factor-α were increased by four- to fivefold, in Npr1 −/− mice hearts compared with control animals. The NF-κB binding activity in nuclear extracts of Npr1 −/− mice hearts was increased by fourfold compared with wild-type Npr1 +/+ mice hearts. Treatments with captopril or hydralazine equally attenuated SBP; however, only captopril significantly decreased the HW/BW ratio and suppressed cytokine gene expression in Npr1 −/− mice hearts. The ventricular cGMP level was reduced by almost sixfold in Npr1 −/− mice compared with wild-type control mice. The results of the present study indicate that disruption of NPRA/cGMP signaling leads to the augmented expression of cardiac RAS pathways that promote the development of cardiac hypertrophy and remodeling.

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