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Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction

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Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction. / Xu, Xin; Zhang, Ping; Kwak, Dongmin; Fassett, John; Yue, Wenhui; Atzler, Dorothee; Hu, Xinli; Liu, Xiaohong; Wang, Huan; Lu, Zhongbing; Guo, Haipeng; Schwedhelm, Edzard; Böger, Rainer H; Chen, Peijie; Chen, Yingjie.

In: BASIC RES CARDIOL, Vol. 112, No. 5, 17.08.2017, p. 55.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Xu, X, Zhang, P, Kwak, D, Fassett, J, Yue, W, Atzler, D, Hu, X, Liu, X, Wang, H, Lu, Z, Guo, H, Schwedhelm, E, Böger, RH, Chen, P & Chen, Y 2017, 'Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction', BASIC RES CARDIOL, vol. 112, no. 5, pp. 55. https://doi.org/10.1007/s00395-017-0644-z

APA

Xu, X., Zhang, P., Kwak, D., Fassett, J., Yue, W., Atzler, D., Hu, X., Liu, X., Wang, H., Lu, Z., Guo, H., Schwedhelm, E., Böger, R. H., Chen, P., & Chen, Y. (2017). Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction. BASIC RES CARDIOL, 112(5), 55. https://doi.org/10.1007/s00395-017-0644-z

Vancouver

Xu X, Zhang P, Kwak D, Fassett J, Yue W, Atzler D et al. Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction. BASIC RES CARDIOL. 2017 Aug 17;112(5):55. https://doi.org/10.1007/s00395-017-0644-z

Bibtex

@article{f906f3f8c152412a8cc5d2371896b5e7,
title = "Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction",
abstract = "Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability. Dimethylarginine dimethylaminohydrolase-1 (DDAH1) exerts a critical role for ADMA degradation and plays an important role in NO signaling. In the heart, DDAH1 is observed in endothelial cells and in the sarcolemma of cardiomyocytes. While NO signaling is important for cardiac adaptation to stress, DDAH1 impact on cardiomyocyte homeostasis is not clear. Here we used the MerCreMer-LoxP model to specifically disrupt cardiomyocyte DDAH1 expression in adult mice to determine the physiological impact of cardiomyocyte DDAH1 under basal conditions and during hypertrophic stress imposed by transverse aortic constriction (TAC). Under control conditions, cardiomyocyte-specific DDAH1 knockout (cDDAH KO) had no detectable effect on plasma ADMA and left ventricular (LV) hypertrophy or function in adult or aging mice. In response to TAC, DDAH1 levels were elevated 2.5-fold in WT mice, which exhibited no change in LV or plasma ADMA content and moderate LV hypertrophy and LV dysfunction. In contrast, cDDAH1 KO mice exposed to TAC showed no increase in LV DDAH1 expression, slightly increased LV tissue ADMA levels, no increase in plasma ADMA, but significantly exacerbated LV hypertrophy, fibrosis, nitrotyrosine production, and LV dysfunction. These findings indicate cardiomyocyte DDAH1 activity is dispensable for cardiac function under basal conditions, but plays an important role in attenuating cardiac hypertrophy and ventricular remodeling under stress conditions, possibly through locally confined regulation of subcellular ADMA and NO signaling.",
keywords = "Journal Article",
author = "Xin Xu and Ping Zhang and Dongmin Kwak and John Fassett and Wenhui Yue and Dorothee Atzler and Xinli Hu and Xiaohong Liu and Huan Wang and Zhongbing Lu and Haipeng Guo and Edzard Schwedhelm and B{\"o}ger, {Rainer H} and Peijie Chen and Yingjie Chen",
year = "2017",
month = aug,
day = "17",
doi = "10.1007/s00395-017-0644-z",
language = "English",
volume = "112",
pages = "55",
journal = "BASIC RES CARDIOL",
issn = "0300-8428",
publisher = "D. Steinkopff-Verlag",
number = "5",

}

RIS

TY - JOUR

T1 - Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction

AU - Xu, Xin

AU - Zhang, Ping

AU - Kwak, Dongmin

AU - Fassett, John

AU - Yue, Wenhui

AU - Atzler, Dorothee

AU - Hu, Xinli

AU - Liu, Xiaohong

AU - Wang, Huan

AU - Lu, Zhongbing

AU - Guo, Haipeng

AU - Schwedhelm, Edzard

AU - Böger, Rainer H

AU - Chen, Peijie

AU - Chen, Yingjie

PY - 2017/8/17

Y1 - 2017/8/17

N2 - Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability. Dimethylarginine dimethylaminohydrolase-1 (DDAH1) exerts a critical role for ADMA degradation and plays an important role in NO signaling. In the heart, DDAH1 is observed in endothelial cells and in the sarcolemma of cardiomyocytes. While NO signaling is important for cardiac adaptation to stress, DDAH1 impact on cardiomyocyte homeostasis is not clear. Here we used the MerCreMer-LoxP model to specifically disrupt cardiomyocyte DDAH1 expression in adult mice to determine the physiological impact of cardiomyocyte DDAH1 under basal conditions and during hypertrophic stress imposed by transverse aortic constriction (TAC). Under control conditions, cardiomyocyte-specific DDAH1 knockout (cDDAH KO) had no detectable effect on plasma ADMA and left ventricular (LV) hypertrophy or function in adult or aging mice. In response to TAC, DDAH1 levels were elevated 2.5-fold in WT mice, which exhibited no change in LV or plasma ADMA content and moderate LV hypertrophy and LV dysfunction. In contrast, cDDAH1 KO mice exposed to TAC showed no increase in LV DDAH1 expression, slightly increased LV tissue ADMA levels, no increase in plasma ADMA, but significantly exacerbated LV hypertrophy, fibrosis, nitrotyrosine production, and LV dysfunction. These findings indicate cardiomyocyte DDAH1 activity is dispensable for cardiac function under basal conditions, but plays an important role in attenuating cardiac hypertrophy and ventricular remodeling under stress conditions, possibly through locally confined regulation of subcellular ADMA and NO signaling.

AB - Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability. Dimethylarginine dimethylaminohydrolase-1 (DDAH1) exerts a critical role for ADMA degradation and plays an important role in NO signaling. In the heart, DDAH1 is observed in endothelial cells and in the sarcolemma of cardiomyocytes. While NO signaling is important for cardiac adaptation to stress, DDAH1 impact on cardiomyocyte homeostasis is not clear. Here we used the MerCreMer-LoxP model to specifically disrupt cardiomyocyte DDAH1 expression in adult mice to determine the physiological impact of cardiomyocyte DDAH1 under basal conditions and during hypertrophic stress imposed by transverse aortic constriction (TAC). Under control conditions, cardiomyocyte-specific DDAH1 knockout (cDDAH KO) had no detectable effect on plasma ADMA and left ventricular (LV) hypertrophy or function in adult or aging mice. In response to TAC, DDAH1 levels were elevated 2.5-fold in WT mice, which exhibited no change in LV or plasma ADMA content and moderate LV hypertrophy and LV dysfunction. In contrast, cDDAH1 KO mice exposed to TAC showed no increase in LV DDAH1 expression, slightly increased LV tissue ADMA levels, no increase in plasma ADMA, but significantly exacerbated LV hypertrophy, fibrosis, nitrotyrosine production, and LV dysfunction. These findings indicate cardiomyocyte DDAH1 activity is dispensable for cardiac function under basal conditions, but plays an important role in attenuating cardiac hypertrophy and ventricular remodeling under stress conditions, possibly through locally confined regulation of subcellular ADMA and NO signaling.

KW - Journal Article

U2 - 10.1007/s00395-017-0644-z

DO - 10.1007/s00395-017-0644-z

M3 - SCORING: Journal article

C2 - 28819685

VL - 112

SP - 55

JO - BASIC RES CARDIOL

JF - BASIC RES CARDIOL

SN - 0300-8428

IS - 5

ER -