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  1. Article ; Online: The Mas agonist CGEN-856S prevents Ang II induced cardiomyocyte hypertrophy via nitric oxide production.

    Nocchi, Eduardo / Scalzo, Sérgio / Rocha-Resende, Cibele / Almeida, Pedro / Parreira, Amanda / Miranda, Kiany / Moura, Victor / Dos Santos, Robson A S / Guatimosim, Silvia

    Peptides

    2024  Volume 175, Page(s) 171182

    Abstract: With the previous knowledge of the cardioprotective effects of the Angiotensin-(1-7) axis, a agonist of Mas receptor has been described, the CGEN-856S. This peptide is more stable than Ang-(1-7), and has a low binding affinity to Angiotensin II receptors. ...

    Abstract With the previous knowledge of the cardioprotective effects of the Angiotensin-(1-7) axis, a agonist of Mas receptor has been described, the CGEN-856S. This peptide is more stable than Ang-(1-7), and has a low binding affinity to Angiotensin II receptors. Although the cardioprotective effects of CGEN-856S were previously shown in vivo, the mechanisms behind its effects are still unknown. Here, we employed a combination of molecular biology, confocal microscopy, and genetically modified mouse with Mas deletion to investigate the CGEN-856S protective signaling in cardiomyocytes. In isolated adult ventricular myocytes, CGEN-856S induced an increase in nitric oxide (NO) production which was absent in cells from Mas knockout mice. Using western blot, we observed a significant increase in phosphorylation of AKT after treatment with CGEN-856S. In addition, CGEN-856S prevented the Ang II induced hypertrophy and the nuclear translocation of GRK5 in a culture model of rat neonatal cardiomyocytes. Blockage of Mas receptor and inhibition of the NO synthase abolished the effects of CGEN-856S on Ang II treated cardiomyocytes. In conclusion, we show that CGEN-856S acting via receptor Mas induces NO raise to block Ang II induced cardiomyocyte hypertrophy. These results indicate that CGEN-856S acts very similarly to Ang-(1-7) in cardiac myocytes, highlighting its therapeutic potential for treating cardiovascular diseases.
    MeSH term(s) Rats ; Mice ; Animals ; Myocytes, Cardiac/metabolism ; Nitric Oxide/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Mas ; Receptors, G-Protein-Coupled/metabolism ; Hypertrophy/metabolism ; Angiotensin II/metabolism
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; Proto-Oncogene Proteins ; Proto-Oncogene Mas ; Receptors, G-Protein-Coupled ; Angiotensin II (11128-99-7)
    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 769028-9
    ISSN 1873-5169 ; 0196-9781
    ISSN (online) 1873-5169
    ISSN 0196-9781
    DOI 10.1016/j.peptides.2024.171182
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1649: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Beneficial effects of angiotensin-(1-7) against deoxycorticosterone acetate-induced diastolic dysfunction occur independently of changes in blood pressure.

    de Almeida, Pedro W Machado / Melo, Marcos Barrouin / Lima, Ricardo de Freitas / Gavioli, Mariana / Santiago, Nivia M / Greco, Leonardo / Jesus, Itamar C G / Nocchi, Eduardo / Parreira, Amanda / Alves, Marcia N M / Mitraud, Luciana / Resende, Rodrigo Ribeiro / Campagnole-Santos, Maria José / Dos Santos, Robson Augusto Souza / Guatimosim, Silvia

    Hypertension (Dallas, Tex. : 1979)

    2015  Volume 66, Issue 2, Page(s) 389–395

    Abstract: Mineralocorticoids have been implicated in the pathogenesis of diastolic heart failure. On the contrary, angiotensin (Ang)-(1-7) has emerged as a potential strategy for treatment of cardiac dysfunction induced by excessive mineralocorticoid receptor ... ...

    Abstract Mineralocorticoids have been implicated in the pathogenesis of diastolic heart failure. On the contrary, angiotensin (Ang)-(1-7) has emerged as a potential strategy for treatment of cardiac dysfunction induced by excessive mineralocorticoid receptor activation. A critical question about the cardioprotective effect of Ang-(1-7) in hypertensive models is its dependence on blood pressure (BP) reduction. Here, we addressed this question by investigating the mechanisms involved in Ang-(1-7) cardioprotection against mineralocorticoid receptor activation. Sprague-Dawley (SD) and transgenic (TG) rats that overexpress an Ang-(1-7) producing fusion protein (TG(A1-7)3292) were treated with deoxycorticosterone acetate (DOCA) for 6 weeks. After treatment, SD rats became hypertensive and developed ventricular hypertrophy. These parameters were attenuated in TG-DOCA. SD-DOCA rats developed diastolic dysfunction which was associated at the cellular level with reduced Ca(2+) transient. Oppositely, TG-DOCA myocytes presented enhanced Ca(2+) transient. Moreover, higher extracellular signal-regulated kinase phosphorylation, type 1 phosphatase, and protein kinase Cα levels were found in SD-DOCA cells. In vivo, pressor effects of DOCA can contribute to the diastolic dysfunction, raising the question of whether protection in TG was a consequence of reduced BP. To address this issue, BP in SD-DOCA was kept at TG-DOCA level by giving hydralazine or by reducing the DOCA amount given to rats (Low-DOCA). Under similar BP, diastolic dysfunction and molecular changes were still evident in DOCA-hydralazine and SD-low-DOCA, but not in TG-DOCA. In conclusion, Ang-(1-7) protective signaling against DOCA-induced diastolic dysfunction occurs independently of BP attenuation and is mediated by the activation of pathways involved in Ca(2+) handling, hypertrophy, and survival.
    MeSH term(s) Angiotensin I/pharmacology ; Angiotensin I/therapeutic use ; Animals ; Blood Pressure/drug effects ; Blood Pressure/physiology ; Calcium/physiology ; Calcium Signaling/drug effects ; Calcium Signaling/physiology ; Desoxycorticosterone Acetate/adverse effects ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Heart Failure, Diastolic/chemically induced ; Heart Failure, Diastolic/physiopathology ; Heart Failure, Diastolic/prevention & control ; Hydralazine/pharmacology ; Hypertension/physiopathology ; Male ; Peptide Fragments/pharmacology ; Peptide Fragments/therapeutic use ; Rats ; Rats, Sprague-Dawley ; Rats, Transgenic
    Chemical Substances Peptide Fragments ; Hydralazine (26NAK24LS8) ; Desoxycorticosterone Acetate (6E0A168OB8) ; Angiotensin I (9041-90-1) ; angiotensin I (1-7) (IJ3FUK8MOF) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2015-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.114.04893
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1488: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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