Molecular cloning of a novel angiotensin II receptor isoform involved in phosphotyrosine phosphatase inhibition.

Kambayashi, Yoshikazu; Bardhan, Smriti; Takahashi, Kyôko; Tsuzuki, Satoshi; Inui, Hiroshi; Hamakubo, Takao; Inagami, Tadashi

doi:10.1016/s0021-9258(19)74499-8

Cited by 656 publications

(72 citation statements)

References 32 publications

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“…72 The AT1R has a calculated mass of 40,889 Daltons as deduced from its 359 amino acid sequence 73,74 and the molecular mass of AT2R is predicated to be 41,346 Daltons based on its 363 amino acid sequence. 75,76 However, the major specific bands of AT1R and AT2R obtained from western blot were larger than the sizes predicted by their amino acid sequences due to the glycosylation of receptor proteins.69 This phenomenon is much more obvious for AT2R. 77,78 Moreover, our data also show that both AT1R and AT2R western blot signals were eliminated by preadsorption of the antibodies with blocking peptides (blots 2–4 for AT2R and blots 6–8 for AT1R, Figure 5), further demonstrating the specificity of the antibodies we used.…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Gao

Chao

Parbhu

et al. 2012

J Renin Angiotensin Aldosterone Syst

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In the current experiment, we determined AT2R and AT1R protein expression by Western blot analysis in developing normal mice. The results indicate that, (1) in all detected brain regions and in the spinal cord, adult mice exhibited significantly higher AT2R expression and lower AT1R expression in total protein extracts compared to fetuses and neonates; (2) other major organs, including heart, lung, liver, and kidney, exhibited the same expression pattern as the brain and spinal cord; (3) reciprocal changes in AT2R and AT1R expression were found in the total protein extracts from the brainstems of mice from one day prenatal to six weeks of age. There was a negative correlation between AT2R and AT1R protein expression; (4) in both membrane and cytosolic fractions from the brainstem, adult mice exhibited higher AT2R and lower AT1R expression than did fetuses and neonates; (5) in the brainstem, there were no significant differences in AT2R and AT1R mRNA levels among fetal, neonatal, and adult mice. The above results reconfirmed our previous finding in rats that adult animals have higher AT2R and lower AT1R expression compared to fetuses and neonates. These data imply an involvement of AT1R in fetal development and of AT2R in adult function.

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Section: Discussionmentioning

confidence: 99%

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Gao

Chao

Parbhu

et al. 2012

J Renin Angiotensin Aldosterone Syst

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“…[4][5][6][7] The actions of Ang II are primarily mediated through AT 1 -and AT 2receptors, both of which are seven-transmembrane G-protein coupled receptors that share approximately 34% homology. 8,9 The cell signalling and physiological effects associated with AT 1receptor activation are currently the most thoroughly defined. The necessity of AT 1 -receptors for normal progression of haematopoiesis was demonstrated by the development of panleukopeania and progenitor cell dysfunction in wildtype mice transplanted with AT 1 -receptor-deficient bone marrow.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II stimulates arachidonic acid release from bone marrow stromal cells

Richmond

Tallant

Gallagher

et al. 2004

J Renin Angiotensin Aldosterone Syst

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Introduction Angiotensin II (Ang II) is recognised as a regulator of haematopoiesis, but its actions within the bone marrow are not fully understood. Support of haematopoiesis by bone marrow stromal cells (MSC) is dependent on factors that include arachidonic acid and macrophage colony stimulating factor (MCSF), both of which are increased by Ang II stimulation in other tissues. To further elucidate the mechanisms of Ang II-regulated haematopoiesis, we determined whether Ang II-stimulation alters arachidonic acid release and MCSF secretion from MSC. Methods Cynomolgus monkey MSC isolated from bone marrow aspirates and the human HS-5 stromal cell line were studied for Ang II-mediated arachidonic acid (AA) release, while secretion of MCSF in response to Ang II was studied in HS-5 cells. Cells were labelled overnight with 3H-AA and the release of 3H-AA was measured in culture medium following 20 minutes stimulation with Ang II, alone or in combination with the AT1- or AT 2-receptor antagonists, losartan and PD 123319, respectively. MCSF secretion into culture medium was measured using an enzyme immunoassay following 24 hours of treatment with Ang II alone or in combination with losartan or PD 123319. Phorbol-myristate-acetate, known to stimulate release of AA and MCSF, was used as a positive control in both experiments. Results In response to Ang II, release of 3H-AA from monkey and human MSC was increased (p<0.05) to 147±4% and 124±3% of control, respectively. The AT1- and AT2-receptor antagonists, losartan and PD 123319, individually reduced Ang II-stimulated 3H-AA release. In contrast, Ang II had no effect on secretion of MCSF from HS-5 cells. Conclusions These results provide mechanistic evidence for Ang II-mediated haematopoiesis through AA release that may, in part, explain Ang II-facilitated recovery of haematopoiesis in experimental myelosuppression and the anaemias associated with Ang II receptor blockade.

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“…AT2R shows β hairpin conformations in the extracellular loop2 (ECL2), forming two disulfide bridges linking N-terminus with ECL3 (Cys 35 -Cys 290 ) and helix III with ECL2 (Cys ). The cDNA reading frame encodes a 363-amino acid protein with an approximate molecular weight of 41 KDa, although the molecular weight varies according to cell types due to differences in glycosylation (Kambayashi et al, 1993;Nakajima et al, 1993).…”

Section: At2r Protein Structurementioning

confidence: 99%

Update on Angiotensin II Subtype 2 Receptor: Focus on Peptide and Nonpeptide Agonists

2021

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Angiotensin II (Ang II) is the most dominant effector component of the renin-angiotensin system (RAS) that generally acts through binding to two main classes of G protein-coupled receptors, namely Ang II subtype-1 receptor (AT1R) and angiotensin II subtype-2 receptor (AT2R). Despite some controversial reports, the activation of AT2R generally antagonizes the effects of Ang II binding on AT1R. Studying AT2R signaling, function, and its specific ligands in cell culture or animal studies have confirmed its beneficial effects throughout the body. These characteristics classify AT2R as part of the protective arm of the RAS that, along with functions of Ang (1-7) through Mas receptor signaling modulates the harmful effects of Ang II on AT1R in the activated classical arm of the RAS. Although Ang II is the primary ligand for AT2R, we have summarized other natural or synthetic peptide and nonpeptide agonists with critical evaluation of their structure, mechanism of action, and biological activity.Significance Statement: AT2R is one of the main components of the RAS and has a significant prospective for mediating the beneficial action of the RAS through its protective arm on the body's homeostasis. Targeting AT2R offers substantial clinical application possibilities for modulating various pathological conditions. This review provided concise information regarding the AT2R peptide and nonpeptide agonists and their potential clinical applications for various diseases.

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Molecular cloning of a novel angiotensin II receptor isoform involved in phosphotyrosine phosphatase inhibition.

Cited by 656 publications

References 32 publications

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Ontogeny of angiotensin type 2 and type 1 receptor expression in mice

Angiotensin II stimulates arachidonic acid release from bone marrow stromal cells

Update on Angiotensin II Subtype 2 Receptor: Focus on Peptide and Nonpeptide Agonists

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