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Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology.
Curr Med Chem. 2015; 22(28):3210-6.CM

Abstract

Exaggerated activation of the renin-angiotensin system via tissue angiotensin II (Ang II) type 1 receptor (AT1R) signaling exerts detrimental effects on cardiovascular, renal and endocrine systems to provoke hypertension and related target organ damage. On the other hand, accumulated research evidence of both basic and clinical studies shows that physiological AT1R signaling also plays an indispensable role for the normal organ development such as the kidney and the maintenance of cardiovascular and renal homeostasis. Such functional diversity of AT1R signaling prompts us to seek a new strategy of selective modulation of AT1R signaling in pathophysiology. In the course of an investigational search for a means to functionally and selectively modulate AT1R signaling for that purpose, a molecule directly interacting with the carboxyl-terminal cytoplasmic domain of AT1R was identified by employing yeast two-hybrid screening of a mouse kidney cDNA library and named AT1R-associated protein (ATRAP). The results of functional analysis showed that ATRAP promotes constitutive AT1R internalization in cultured cells and inhibits Ang II-mediated pathological response in mouse distal convoluted cells. The ATRAP is expressed in a variety of tissues including the kidney where ATRAP is abundantly distributed in epithelial cells along the renal tubules. The results employing genetic engineered mice with modified ATRAP expression showed that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli such as chronic Ang II infusion, and suggest ATRAP to be a target of interest.

Authors+Show Affiliations

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. tamukou@med.yokohama-cu.ac.jp.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

26295465

Citation

Tamura, K, et al. "Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology." Current Medicinal Chemistry, vol. 22, no. 28, 2015, pp. 3210-6.
Tamura K, Wakui H, Azushima K, et al. Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology. Curr Med Chem. 2015;22(28):3210-6.
Tamura, K., Wakui, H., Azushima, K., Uneda, K., Haku, S., Kobayashi, R., Ohki, K., Haruhara, K., Kinguchi, S., Matsuda, M., Yamashita, A., & Umemura, S. (2015). Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology. Current Medicinal Chemistry, 22(28), 3210-6.
Tamura K, et al. Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology. Curr Med Chem. 2015;22(28):3210-6. PubMed PMID: 26295465.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology. AU - Tamura,K, AU - Wakui,H, AU - Azushima,K, AU - Uneda,K, AU - Haku,S, AU - Kobayashi,R, AU - Ohki,K, AU - Haruhara,K, AU - Kinguchi,S, AU - Matsuda,M, AU - Yamashita,A, AU - Umemura,S, PY - 2015/07/01/received PY - 2015/08/19/revised PY - 2015/08/20/accepted PY - 2015/8/22/entrez PY - 2015/8/22/pubmed PY - 2016/4/9/medline SP - 3210 EP - 6 JF - Current medicinal chemistry JO - Curr. Med. Chem. VL - 22 IS - 28 N2 - Exaggerated activation of the renin-angiotensin system via tissue angiotensin II (Ang II) type 1 receptor (AT1R) signaling exerts detrimental effects on cardiovascular, renal and endocrine systems to provoke hypertension and related target organ damage. On the other hand, accumulated research evidence of both basic and clinical studies shows that physiological AT1R signaling also plays an indispensable role for the normal organ development such as the kidney and the maintenance of cardiovascular and renal homeostasis. Such functional diversity of AT1R signaling prompts us to seek a new strategy of selective modulation of AT1R signaling in pathophysiology. In the course of an investigational search for a means to functionally and selectively modulate AT1R signaling for that purpose, a molecule directly interacting with the carboxyl-terminal cytoplasmic domain of AT1R was identified by employing yeast two-hybrid screening of a mouse kidney cDNA library and named AT1R-associated protein (ATRAP). The results of functional analysis showed that ATRAP promotes constitutive AT1R internalization in cultured cells and inhibits Ang II-mediated pathological response in mouse distal convoluted cells. The ATRAP is expressed in a variety of tissues including the kidney where ATRAP is abundantly distributed in epithelial cells along the renal tubules. The results employing genetic engineered mice with modified ATRAP expression showed that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli such as chronic Ang II infusion, and suggest ATRAP to be a target of interest. SN - 1875-533X UR - https://www.unboundmedicine.com/medline/citation/26295465/Angiotensin_II_Type_1_Receptor_Binding_Molecule_ATRAP_as_a_Possible_Modulator_of_Renal_Sodium_Handling_and_Blood_Pressure_in_Pathophysiology_ L2 - http://www.eurekaselect.com/134204/article DB - PRIME DP - Unbound Medicine ER -