The role of angiotensin II in the feedback control of renin gene expression

1997 ◽  
Vol 434 (2) ◽  
pp. 166-172 ◽  
Author(s):  
Karin Schricker ◽  
Stephan Holmer ◽  
Bernhard K. Krämer ◽  
Günter A. J. Riegger ◽  
A. Kurtz
2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Wendy Rosales ◽  
Juan Carulla ◽  
Jeison García ◽  
Diana Vargas ◽  
Fernando Lizcano

Epigenetic changes induced by histone demethylases play an important role in differentiation and pathological changes in cardiac cells. However, the role of the jumonji family of demethylases in the development of cardiac hypertrophy remains elusive. In this study, the presence of different histone demethylases in cardiac cells was evaluated after hypertrophy was induced with neurohormones. A cell line from rat cardiomyocytes was used as a biological model. The phenotypic profiles of the cells, as well as the expression of histone demethylases, were studied through immunofluorescence, transient transfection, western blot, and qRT-PCR analysis after inducing hypertrophy by angiotensin II and endothelin-1. An increase in fetal gene expression (ANP, BNP, andβ-MHC) was observed in cardiomyocytes after treatment with angiotensin II and endothelin-1. A significant increase in JMJD2A expression, but not in UTX or JMJD2C expression, was observed. When JMJD2A was overexpressed in cardiomyocytes through transient transfection, the effect of neurohormones on fetal cardiac gene expression was increased. We conclude that JMJD2A plays a principal role in the regulation of fetal cardiac genes, which increase in expression during the pathological hypertrophic process.


1992 ◽  
Vol 262 (3) ◽  
pp. R459-R463 ◽  
Author(s):  
W. V. Page ◽  
S. Perlman ◽  
F. G. Smith ◽  
J. L. Segar ◽  
J. E. Robillard

The role of renal nerves in regulating changes in plasma renin activity (PRA) and renal renin gene expression was studied in intact (n = 6) and denervated (n = 6) fetal sheep before birth and during the first 24 h after delivery. Renal denervation completely blunted the rise in PRA observed 24 h after delivery in newborn lambs; in lambs with intact kidneys, PRA increased significantly (P less than 0.05) from 3.26 +/- 0.60 (predelivery) to 6.34 +/- 1.85 ng angiotensin I (ANG I).ml-1.h-1 (24 h postdelivery), while in lambs with denervated kidneys, predelivery and post-delivery values were 2.84 +/- 0.19 and 2.49 +/- 0.45 ng ANG I.ml-1.h-1, respectively. Renin mRNA levels were significantly lower (P less than 0.001) in denervated than in intact kidneys 24 h after birth. A close analysis of these results also revealed that renin mRNA levels were significantly higher (P less than 0.001) in intact kidneys of newborn lambs delivered vaginally (n = 3) than in newborn lambs delivered by cesarean section (n = 3). These results suggest that renal nerves play an important role in regulating renin gene expression and PRA during the transition from fetal to newborn life.


Peptides ◽  
2004 ◽  
Vol 25 (7) ◽  
pp. 1107-1114 ◽  
Author(s):  
Hisamitsu Onitsuka ◽  
Takuroh Imamura ◽  
Kaoru Ito ◽  
Kenji Kuwasako ◽  
Hiroshi Yamakawa ◽  
...  

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Wen Jin ◽  
Marpadga A Reddy ◽  
Zhuo Chen ◽  
Sadhan Das ◽  
Linda Lanting ◽  
...  

Angiotensin II (Ang II)-mediated vascular smooth muscle cell (VSMC) dysfunction plays a critical role in the pathogenesis of Cardiovascular Diseases (CVDs). However, the role of Ang II-induced transcription factors in the diverse effects of Ang II remains unclear. We profiled Ang II induced gene expression by microarray analysis of RNA isolated from Ang II-treated and control VSMC. Our results identified numerous differentially regulated genes including several key transcription factors in Ang II-stimulated VSMC compared with controls. Ingenuity Pathway Analysis indicated that Ang II-regulated genes are involved in VSMC dysfunction highly relevant to CVDs. We validated the expression of several genes by RT-qPCR and further characterized the functions of the most differentially regulated gene, KLF4, known to regulate growth factor induced VSMC phenotypic switching. We demonstrated that Ang II induced the expression of KLF4 in cultured VSMC in vitro , in mice aortas cultured ex vivo , and in aortas isolated from Ang II-infused mice in vivo . Ang II-induced KLF4 expression was inhibited by Losartan, demonstrating regulation via the AT1 receptor. Transfection experiments using WT and mutant KLF4 promoter constructs revealed the key role of cis -elements with consensus binding sites for p53, SP1 and YY1 in Ang II-induced KLF4 promoter activation. Next, we performed gene expression profiling by Affymetrix gene arrays after siRNA mediated KLF4 knockdown in VSMC. The differentially expressed genes were subsequently analyzed by DAVID to obtain enriched biological processes and potential pathways relevant to cardiovascular functions. Results showed that KLF4 knockdown upregulated the expression of several genes related to cell proliferation and hypertrophy. Interestingly, KLF4 knockdown also enhanced the expression of multiple pro-inflammatory genes including IL-6 and downregulated several anti-inflammatory genes including Thrombomodulin, suggesting an anti-inflammatory role for KLF4 in VSMC. Together, these results suggest that KLF4 may act as a novel molecular brake to modulate Ang II actions that, when disrupted, can further augment Ang II mediated VSMC dysfunction associated with vascular diseases.


1994 ◽  
Vol 427 (1-2) ◽  
pp. 42-46 ◽  
Author(s):  
Karin Schricker ◽  
Marlies Hamann ◽  
Brigitte Kaissling ◽  
Armin Kurtz

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