Abstract
The Ang II type 1 receptor (AT1R)-associated protein (ATRAP/Agtrap) is a molecule specifically interacting with the carboxyl- terminal domain of AT1R. The results of in vitro studies showed that ATRAP suppresses Ang II-mediated pathological responses in cardiovascular cells by promoting AT1R internalization. With respect to the tissue distribution and regulation of ATRAP expression in vivo, ATRAP is broadly expressed in many tissues as is AT1R. Accumulating evidence indicates that a tissue-specific regulatory balancing of ATRAP and AT1R expression may be involved in the modulation of AT1R signaling at local tissue sites and also in the pathophysiology of hypertension and its associated end-organ injury. Furthermore, the activation of ATRAP in transgenic-models inhibited inflammatory vascular remodeling and cardiac hypertrophy in response to Ang II stimulation. These results suggest the clinical potential benefit of an ATRAP activation strategy in the treatment of hypertension and related organ injury.
Keywords: Gene expression/regulation, hypertension, receptor internalization, receptor signaling, renin-angiotensin system, target organ injury.
Current Pharmaceutical Design
Title:The Physiology and Pathophysiology of a Novel Angiotensin Receptor-binding Protein ATRAP/Agtrap
Volume: 19 Issue: 17
Author(s): Shin-ichiro Masuda, Satoshi Umemura, Akio Yamashita, Yasuo Tokita, Yoshiyuki Toya, Miyuki Matsuda, Yuko Tsurumi-Ikeya, Yuichi Koide, Atsu-ichiro Shigenaga, Koichi Azuma, Kouichi Tamura, Kazushi Uneda, Sona Haku, Tomohiko Kanaoka, Kengo Azushima, Masato Ohsawa, Toru Dejima, Akinobu Maeda and Hiromichi Wakui
Affiliation:
Keywords: Gene expression/regulation, hypertension, receptor internalization, receptor signaling, renin-angiotensin system, target organ injury.
Abstract: The Ang II type 1 receptor (AT1R)-associated protein (ATRAP/Agtrap) is a molecule specifically interacting with the carboxyl- terminal domain of AT1R. The results of in vitro studies showed that ATRAP suppresses Ang II-mediated pathological responses in cardiovascular cells by promoting AT1R internalization. With respect to the tissue distribution and regulation of ATRAP expression in vivo, ATRAP is broadly expressed in many tissues as is AT1R. Accumulating evidence indicates that a tissue-specific regulatory balancing of ATRAP and AT1R expression may be involved in the modulation of AT1R signaling at local tissue sites and also in the pathophysiology of hypertension and its associated end-organ injury. Furthermore, the activation of ATRAP in transgenic-models inhibited inflammatory vascular remodeling and cardiac hypertrophy in response to Ang II stimulation. These results suggest the clinical potential benefit of an ATRAP activation strategy in the treatment of hypertension and related organ injury.
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Cite this article as:
Masuda Shin-ichiro, Umemura Satoshi, Yamashita Akio, Tokita Yasuo, Toya Yoshiyuki, Matsuda Miyuki, Tsurumi-Ikeya Yuko, Koide Yuichi, Shigenaga Atsu-ichiro, Azuma Koichi, Tamura Kouichi, Uneda Kazushi, Haku Sona, Kanaoka Tomohiko, Azushima Kengo, Ohsawa Masato, Dejima Toru, Maeda Akinobu and Wakui Hiromichi, The Physiology and Pathophysiology of a Novel Angiotensin Receptor-binding Protein ATRAP/Agtrap, Current Pharmaceutical Design 2013; 19 (17) . https://dx.doi.org/10.2174/1381612811319170010
DOI https://dx.doi.org/10.2174/1381612811319170010 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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