What question did this study set out to answer?

To investigate whether the dual-specificity phosphatase MKP-1 regulates cardiac mitogen-activated protein kinase signaling pathways and attenuates cardiac hypertrophy in vitro and in vivo.

January 19, 2001Circulation ResearchOpen Access

The Dual-Specificity Phosphatase MKP-1 Limits the Cardiac Hypertrophic Response In Vitro and In Vivo

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Authors

OBOrlando F. BuenoAbbVie (United States)LWLeón J. De WindtHeart Failure & Transplant HLHae W. LimMedtronic (Ireland)

Discussion

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Overview

Preclinical study reveals that MKP-1 overexpression prevents pathological cardiac hypertrophy in murine models, highlighting dual-specificity phosphatases as critical heart growth regulators.

Key Points

To investigate whether the dual-specificity phosphatase MKP-1 regulates cardiac mitogen-activated protein kinase signaling pathways and attenuates cardiac hypertrophy in vitro and in vivo.
Cultured primary cardiomyocytes were transduced via adenovirus-mediated gene transfer to constitutively express MKP-1 during agonist-induced hypertrophy.
Transgenic mice engineered to express physiological levels of cardiac MKP-1 were evaluated at baseline and following aortic banding or chronic catecholamine infusion.
Constitutive expression of MKP-1 in primary cardiomyocytes completely blocked agonist-induced activation of p38, JNK1/2, and ERK1/2 and prevented cellular hypertrophy.
Transgenic mice exhibited absent p38, JNK1/2, and ERK1/2 activation, reduced developmental myocardial growth, and significantly attenuated hypertrophic responses to aortic banding and catecholamines.

Cite This Study

Bueno et al. (2001) studied this question.

synapsesocial.com/papers/6a6ff6ac6ceb2bbd16dfc377 https://doi.org/10.1161/01.res.88.1.88

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January 19, 2001Circulation ResearchOpen Access

The Dual-Specificity Phosphatase MKP-1 Limits the Cardiac Hypertrophic Response In Vitro and In Vivo

View Full Paper

Ask AI

Bookmark

Authors

OBOrlando F. BuenoAbbVie (United States)LWLeón J. De WindtHeart Failure & Transplant HLHae W. LimMedtronic (Ireland)

Discussion

Member takes

Overview

Preclinical study reveals that MKP-1 overexpression prevents pathological cardiac hypertrophy in murine models, highlighting dual-specificity phosphatases as critical heart growth regulators.

Key Points

To investigate whether the dual-specificity phosphatase MKP-1 regulates cardiac mitogen-activated protein kinase signaling pathways and attenuates cardiac hypertrophy in vitro and in vivo.
Cultured primary cardiomyocytes were transduced via adenovirus-mediated gene transfer to constitutively express MKP-1 during agonist-induced hypertrophy.
Transgenic mice engineered to express physiological levels of cardiac MKP-1 were evaluated at baseline and following aortic banding or chronic catecholamine infusion.
Constitutive expression of MKP-1 in primary cardiomyocytes completely blocked agonist-induced activation of p38, JNK1/2, and ERK1/2 and prevented cellular hypertrophy.
Transgenic mice exhibited absent p38, JNK1/2, and ERK1/2 activation, reduced developmental myocardial growth, and significantly attenuated hypertrophic responses to aortic banding and catecholamines.

Cite This Study

Bueno et al. (2001) studied this question.

synapsesocial.com/papers/6a6ff6ac6ceb2bbd16dfc377 https://doi.org/10.1161/01.res.88.1.88

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