Importance of Tyrosine Phosphorylation in Angiotensin II Type 1 Receptor Signaling

Hypertension ◽  
1996 ◽  
Vol 27 (3) ◽  
pp. 476-480 ◽  
Author(s):  
Bernhard Schieffer ◽  
William G. Paxton ◽  
Mario B. Marrero ◽  
Kenneth E. Bernstein
Diabetes ◽  
2008 ◽  
Vol 57 (8) ◽  
pp. 2191-2198 ◽  
Author(s):  
T. Kurihara ◽  
Y. Ozawa ◽  
N. Nagai ◽  
K. Shinoda ◽  
K. Noda ◽  
...  

2007 ◽  
Vol 18 (4) ◽  
pp. 1140-1149 ◽  
Author(s):  
Bing Shen ◽  
Lisa M. Harrison-Bernard ◽  
Andrew J. Fuller ◽  
Vanessa Vanderpool ◽  
Zubaida Saifudeen ◽  
...  

2014 ◽  
Vol 289 (41) ◽  
pp. 28271-28283 ◽  
Author(s):  
Wei Tang ◽  
Ryan T. Strachan ◽  
Robert J. Lefkowitz ◽  
Howard A. Rockman

2007 ◽  
Vol 292 (5) ◽  
pp. H2306-H2315 ◽  
Author(s):  
Mami Ishikawa ◽  
Eiichi Sekizuka ◽  
Noriyuki Yamaguchi ◽  
Hiromichi Nakadate ◽  
Satoshi Terao ◽  
...  

Angiotensin II type 1 (AT1) receptor signaling has been implicated in cerebral microvascular alterations associated with ischemia, diabetes mellitus, hypercholesterolemia, and atherosclerosis. Platelets, which express AT1 receptors, also appear to contribute to the thrombogenic and inflammatory responses that are elicited by these pathological conditions. This study assesses the role of AT1 receptor activation on platelet-leukocyte-endothelial cell interactions elicited in cerebral microvasculature by ischemia and reperfusion. Intravital microscopy was used to monitor the adhesion of platelets and leukocytes that were labeled with different fluorochromes, whereas dihydrorhodamine-123 was used to quantify oxygen radical production in cerebral surface of mice that were either treated with the AT1 receptor agonist Val-angiotensin II (ANG II) or subjected to bilateral common carotid artery occlusion (BCCAO) followed by reperfusion. ANG II elicited a dose- and time- dependent increase in platelet-leukocyte-endothelial cell interactions in cerebral venules that included rolling platelets, adherent platelets on the leukocytes and the endothelial cells, rolling leukocytes, and adherent leukocytes. All of these interactions were attenuated by treatment with either P-selectin or P-selectin glycoprotein ligand 1 (PSGL-1) antibody. The AT1 receptor antagonist candesartan and losartan as well as diphenyleneiodonium, an inhibitor of flavoproteins including NAD(P)H oxidase, significantly reduced the platelet-leukocyte-endothelial cell interactions elicited by either ANG II administration or BCCAO/reperfusion. The increased oxygen radical generation elicited by BCCAO/reperfusion was also attenuated by candesartan. These findings are consistent with an AT1 receptor signaling mechanism, which involves oxygen radical production and ultimately results in P-selectin- and PSGL-1-mediated platelet-leukocyte-endothelial cell interactions in the cerebral microcirculation


2006 ◽  
Vol 4 (1) ◽  
pp. 67-78 ◽  
Author(s):  
Hidekatsu Nakashima ◽  
Hiroyuki Suzuki ◽  
Haruhiko Ohtsu ◽  
James Chao ◽  
Hirotoshi Utsunomiya ◽  
...  

2014 ◽  
Vol 91 (1) ◽  
Author(s):  
Vijayakumar Chinnathambi ◽  
Amar S. More ◽  
Gary D. Hankins ◽  
Chandra Yallampalli ◽  
Kunju Sathishkumar

2010 ◽  
Vol 299 (4) ◽  
pp. F720-F731 ◽  
Author(s):  
Shin-ichiro Masuda ◽  
Kouichi Tamura ◽  
Hiromichi Wakui ◽  
Akinobu Maeda ◽  
Toru Dejima ◽  
...  

The intrarenal renin-angiotensin system plays a crucial role in the regulation of renal circulation and sodium reabsorption through the activation of vascular, glomerular, and tubular angiotensin II type 1 (AT1) receptor signaling. We previously cloned a molecule that specifically interacted with the murine AT1 receptor to inhibit AT1 receptor signaling, which we named ATRAP (for AT1 receptor-associated protein). Since murine ATRAP was shown to be highly expressed in the kidney, in the present study we investigated expression and distribution of human ATRAP in normal kidney and renal biopsy specimens from patients with IgA nephropathy. In the normal human kidney, both ATRAP mRNA and protein were widely and abundantly distributed along the renal tubules from Bowman's capsule to the medullary collecting ducts. In all renal tubular epithelial cells, the ATRAP protein colocalized with the AT1 receptor. In renal biopsy specimens with IgA nephropathy, a significant positive correlation between ATRAP and AT1 receptor gene expression was observed. There was also a positive relationship between tubulointerstitial ATRAP expression and the estimated glomerular filtration rate in patients with IgA nephropathy. Furthermore, we examined the function of the tubular AT1 receptor using an immortalized cell line of mouse distal convoluted tubule cells (mDCT) and found that overexpression of ATRAP by adenoviral gene transfer suppressed the angiotensin II-mediated increases in transforming growth factor-β production in mDCT cells. These findings suggest that ATRAP might play a role in balancing the renal renin-angiotensin system synergistically with the AT1 receptor by counterregulatory effects in IgA nephropathy and propose an antagonistic effect of tubular ATRAP on AT1 receptor signaling.


2011 ◽  
Vol 108 (9) ◽  
pp. 1102-1111 ◽  
Author(s):  
Rosario Scalia ◽  
Yulan Gong ◽  
Brett Berzins ◽  
Brin Freund ◽  
Danielle Feather ◽  
...  

2021 ◽  
Vol 99 (1) ◽  
pp. 148-160 ◽  
Author(s):  
Daniel E. Leisman ◽  
Tiago D. Fernandes ◽  
Vanesa Bijol ◽  
Mabel N. Abraham ◽  
Jake R. Lehman ◽  
...  

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