scholarly journals The novel angiotensin II type 1 receptor (AT1R)-associated protein ATRAP downregulates AT1R and ameliorates cardiomyocyte hypertrophy

FEBS Letters ◽  
2005 ◽  
Vol 579 (7) ◽  
pp. 1579-1586 ◽  
Author(s):  
Yutaka Tanaka ◽  
Kouichi Tamura ◽  
Yuichi Koide ◽  
Masashi Sakai ◽  
Yuko Tsurumi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiomyocyte Hypertrophy ◽  
The Novel

scholarly journals Angiotensin-II type 1 receptor and NOX2 mediate TCF/LEF and CREB dependent WISP1 induction and cardiomyocyte hypertrophy

2011 ◽  
Vol 50 (6) ◽  
pp. 928-938 ◽  
Author(s):  
Prakashsrinivasan Shanmugam ◽  
Anthony J. Valente ◽  
Sumanth D. Prabhu ◽  
Balachandar Venkatesan ◽  
Tadashi Yoshida ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiomyocyte Hypertrophy

scholarly journals High-Salt Intake Induces Cardiomyocyte Hypertrophy in Rats in Response to Local Angiotensin II Type 1 Receptor Activation

2014 ◽  
Vol 144 (10) ◽  
pp. 1571-1578 ◽  
Author(s):  
Isis A. Katayama ◽  
Rafael C. Pereira ◽  
Ellen P. B. Dopona ◽  
Maria H. M. Shimizu ◽  
Luzia N. S. Furukawa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Receptor Activation ◽  
High Salt ◽  
Cardiomyocyte Hypertrophy ◽  
High Salt Intake

scholarly journals Thyroid Hormone Increases TGF-β1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Gabriela Placoná Diniz ◽  
Marcela Sorelli Carneiro-Ramos ◽  
Maria Luiza Morais Barreto-Chaves
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Angiotensin Ii Receptors ◽  
Cardiomyocyte Hypertrophy ◽  
Tgf Β1

TH-induced cardiac hypertrophyin vivois accompanied by increased cardiac Transforming Growth Factor-β1 (TGF-β1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-β1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated withT3did not show alteration on TGF-β1 expression. However, cardiomyocytes treated withT3presented an increase in TGF-β1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented theT3-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. TheT3-induced increase on TGF-β1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated inT3-induced increase on TGF-βexpression and suggest that the trophic effects exerted byT3on cardiomyocytes are not dependent on the higher TGF-β1 levels, since the AT1R and AT2R blockers were able to attenuate theT3-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-β1 levels promoted byT3.

Angiotensin II Type-1 Receptor-JAK/STAT Pathway Mediates the Induction of Visfatin in Angiotensin II-Induced Cardiomyocyte Hypertrophy

2012 ◽  
Vol 343 (3) ◽  
pp. 220-226 ◽  
Author(s):  
Liang Chang ◽  
Rong Yang ◽  
Mei Wang ◽  
Jinming Liu ◽  
Yaling Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiomyocyte Hypertrophy ◽  
Stat Pathway

scholarly journals Identification of Amino Acid Residues in Angiotensin II Type 1 Receptor Sensing Mechanical Stretch and Function in Cardiomyocyte Hypertrophy

2015 ◽  
Vol 37 (1) ◽  
pp. 105-116 ◽  
Author(s):  
Guoliang Jiang ◽  
Hui Gong ◽  
Yuhong Niu ◽  
Chunjie Yang ◽  
Shijun Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mechanical Stretch ◽  
Cardiomyocyte Hypertrophy ◽  
Amino Acid Residues ◽  
Sectional Area ◽  
Cross Sectional ◽  
Cellular Events ◽  
Genes Expression ◽  
And Function

Background/Aims: Angiotensin II (AngII) type 1 receptor (AT1R) could be activated by mechanical stress without the involvement of AngII during the development of cardiac hypertrophy. We aimed to identify sensing sites of AT1R for activation by mechanical stretch. Methods: We constructed several site-directed mutations of AT1R (AT1RK199Q, AT1RL212F, AT1RQ257A and AT1RC289A), transfected them respectively into COS7 cells or angiotensinogen knockout cardiomyocytes (ATG−/−-CMs), and observed cellular events after mechanical stretch. Results: AngII-induced phosphorylation of ERKs and Jak2, and redistribution of Gαq11 in AT1RWT- COS7 or -ATG−/−-CMs were dramatically decreased in AT1RK199Q- or AT1RQ257A- COS7 cells or -ATG−/−-CMs, while those effects induced by mechanical stretch were greatly suppressed in COS7 cells or ATG−/−-CMs expressing AT1RL212F, AT1RQ257A or AT1RC289A compared with these cells expressing AT1RWT. AngII-induced hypertrophic responses (the increase in hypertrophic genes expression and cross-sectional area) in AT1RWT- ATG−/−-CMs were partly abolished in AT1RK199Q-ATG−/−-CMs or AT1RQ257A-ATG−/−-CMs, while these responses induced by mechanical stretch were greatly inhibited in ATG−/−-CMs overexpressing AT1RL212F, AT1RQ257A or AT1RC289A. Conclusion: These results indicated that Leu212, Gln257 and Cys289 in AT1R are not only sensing sites for mechanical stretch but also functional amino residues for activation of the receptor and cardiomyocytes hypertrophy induced by mechanical stretch.

scholarly journals Src Is Required for Mechanical Stretch-Induced Cardiomyocyte Hypertrophy through Angiotensin II Type 1 Receptor-Dependent β-Arrestin2 Pathways

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e92926 ◽  
Author(s):  
Shijun Wang ◽  
Hui Gong ◽  
Guoliang Jiang ◽  
Yong Ye ◽  
Jian Wu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mechanical Stretch ◽  
Cardiomyocyte Hypertrophy
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