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15 results on '"da Costa Goncalves, Andrey C."'

2. The longevity gene mIndy (I'm Not Dead, Yet) affects blood pressure through sympathoadrenal mechanisms

Author

Willmes, Diana M., Daniels, Martin, Kurzbach, Anica, Lieske, Stefanie, Bechmann, Nicole, Schumann, Tina, Henke, Christine, El-Agroudy, Nermeen N., Da Costa Goncalves, Andrey C., Peitzsch, Mirko, Hofmann, Anja, Kanczkowski, Waldemar, Kraeker, Kristin, Mueller, Dominik N., Morawietz, Henning, Deussen, Andreas, Wagner, Michael, El-Armouche, Ali, Helfand, Stephen L., Bornstein, Stephan R., de Cabo, Rafael, Bernier, Michel, Eisenhofer, Graeme, Tank, Jens, Jordan, Jens, Birkenfeld, Andreas L., Willmes, Diana M., Daniels, Martin, Kurzbach, Anica, Lieske, Stefanie, Bechmann, Nicole, Schumann, Tina, Henke, Christine, El-Agroudy, Nermeen N., Da Costa Goncalves, Andrey C., Peitzsch, Mirko, Hofmann, Anja, Kanczkowski, Waldemar, Kraeker, Kristin, Mueller, Dominik N., Morawietz, Henning, Deussen, Andreas, Wagner, Michael, El-Armouche, Ali, Helfand, Stephen L., Bornstein, Stephan R., de Cabo, Rafael, Bernier, Michel, Eisenhofer, Graeme, Tank, Jens, Jordan, Jens, and Birkenfeld, Andreas L.

Abstract

Reduced expression of the plasma membrane citrate transporter INDY (acronym I'm Not Dead, Yet) extends life span in lower organisms. Deletion of the mammalian Indy (mIndy) gene in rodents improves metabolism via mechanisms akin to caloric restriction, known to lower blood pressure {BP) by sympathoadrenal inhibition. We hypothesized that mIady deletion attenuates sympathoadrenal support of BP. Continuous arterial BP and heart rate (HR) were reduced in mINDY-KO mice. Concomitantly, urinary catecholamine content was lower, and the decreases in BP and HR by mIndy deletion were attenuated after autonomic ganglionic blockade. Catecholamine biosynthesis pathways were reduced in mINDY-KO adrenals using unbiased microarray analysis. Citrate, the main mINDY substrate, increased catecholamine content in pheochromocytoma cells, while pharmacological inhibition of citrate uptake blunted the effect. Our data suggest that deletion of mIndy reduces sympathoadrenal support of BP and HR by attenuating catecholamine biosynthesis. Deletion of mIndy recapitulates beneficial cardiovascular and metabolic responses to caloric restriction, making it an attractive therapeutic target.

Published
2021

6. The longevity gene mIndy (I’m Not Dead, Yet) affects blood pressure through sympathoadrenal mechanisms

Author

Willmes, Diana M., primary, Daniels, Martin, additional, Kurzbach, Anica, additional, Lieske, Stefanie, additional, Bechmann, Nicole, additional, Schumann, Tina, additional, Henke, Christine, additional, El-Agroudy, Nermeen N., additional, Da Costa Goncalves, Andrey C., additional, Peitzsch, Mirko, additional, Hofmann, Anja, additional, Kanczkowski, Waldemar, additional, Kräker, Kristin, additional, Müller, Dominik N., additional, Morawietz, Henning, additional, Deussen, Andreas, additional, Wagner, Michael, additional, El-Armouche, Ali, additional, Helfand, Stephen L., additional, Bornstein, Stephan R., additional, de Cabo, Rafael, additional, Bernier, Michel, additional, Eisenhofer, Graeme, additional, Tank, Jens, additional, Jordan, Jens, additional, and Birkenfeld, Andreas L., additional

Published
2021
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8. C-type natriuretic peptide and natriuretic peptide receptor B signalling inhibits cardiac sympathetic neurotransmission and autonomic function

Author

Buttgereit, Jens, primary, Shanks, Julia, additional, Li, Dan, additional, Hao, Guoliang, additional, Athwal, Arvinder, additional, Langenickel, Thomas H., additional, Wright, Hannah, additional, da Costa Goncalves, Andrey C., additional, Monti, Jan, additional, Plehm, Ralph, additional, Popova, Elena, additional, Qadri, Fatimunnisa, additional, Lapidus, Irina, additional, Ryan, Brent, additional, Özcelik, Cemil, additional, Paterson, David J., additional, Bader, Michael, additional, and Herring, Neil, additional

Published
2016
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10. Estrogen Receptor-β Signals Left Ventricular Hypertrophy Sex Differences in Normotensive Deoxycorticosterone Acetate-Salt Mice

Author

Gürgen, Dennis, primary, Hegner, Björn, additional, Kusch, Angelika, additional, Catar, Rusan, additional, Chaykovska, Lyubov, additional, Hoff, Uwe, additional, Gross, Volkmar, additional, Slowinski, Torsten, additional, da Costa Goncalves, Andrey C., additional, Kintscher, Ulrich, additional, Gustafsson, Jan-Åke, additional, Luft, Friedrich C., additional, and Dragun, Duska, additional

Published
2011
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14. Deoxycorticosterone Acetate-Salt Mice Exhibit Blood Pressure–Independent Sexual Dimorphism

Author

Karatas, Aysun, primary, Hegner, Björn, additional, de Windt, Leon J., additional, Luft, Friedrich C., additional, Schubert, Carola, additional, Gross, Volkmar, additional, Akashi, Yoshihiro J., additional, Gürgen, Dennis, additional, Kintscher, Ulrich, additional, da Costa Goncalves, Andrey C., additional, Regitz-Zagrosek, Vera, additional, and Dragun, Duska, additional

Published
2008
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15. Estrogen receptor-beta signals left ventricular hypertrophy sex differences in normotensive deoxycorticosterone acetate-salt mice.

Author

Gürgen, Dennis, Hegner, Björn, Kusch, Angelika, Catar, Rusan, Claykovska, Lyubov, Hoff, Uwe, Gross, Volkmar, Slowinski, Torsten, Goncalves, Andrey C. da Costa, Kintscher, Ulrich, Gustafsson, Jan-Åke, Luft, Friedrich C., Dragun, Duska, Gürgen, Dennis, Hegner, Björn, Chaykovska, Lyubov, da Costa Goncalves, Andrey C, and Gustafsson, Jan-Åke

Abstract

We found earlier that deoxycorticosterone acetate-salt treatment causes blood pressure-independent left ventricular hypertrophy, but only in male mice. To test the hypothesis that the estrogen receptor-β (ERβ) protects the females from left ventricular hypertrophy, we treated male and female ERβ-deficient (ERβ(-/-)) mice and their male and female littermates (wild-type [WT]) with deoxycorticosterone acetate-salt and made them telemetrically normotensive with hydralazine. WT males had increased (+16%) heart weight/tibia length ratios compared with WT females (+7%) at 6 weeks. In ERβ(-/-) mice, this situation was reversed. Female WT mice had the greatest heart weight/tibia length ratio increases of all of the groups (+23%), even greater than ERβ(-/-) males (+10%). Echocardiography revealed concentric left ventricular hypertrophy in male WT mice, whereas ERβ(-/-) females developed dilative left ventricular hypertrophy. The hypertrophic response in female ERβ(-/-) mice was accompanied by the highest degree of collagen deposition, indicating maladaptive remodeling. ERβ(+/+) females showed robust protective p38 and extracellular signal-regulated kinase 1/2 signaling relationships compared with other groups. Calcineurin Aβ expression and its positive regulator myocyte-enriched calcineurin-interacting protein 1 were increased in deoxycorticosterone acetate-salt female ERβ(-/-) mice, yet lower than in WT males. Endothelin increased murine cardiomyocyte hypertrophy in vitro, which could be blocked by estradiol and an ERβ agonist. We conclude that a functional ERβ is essential for inducing adaptive p38 and extracellular signal-regulated kinase signaling, while reducing maladaptive calcineurin signaling in normotensive deoxycorticosterone acetate female mice. Our findings address the possibility of sex-specific cardiovascular therapies. [ABSTRACT FROM AUTHOR]

Published
2011
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