Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor.

Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Research Abstract Details 

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Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Abstract Text:

Pallavi S Peter,Jennifer E Brady,Lin Yan,Wei Chen,Stefan Engelhardt,Yibin Wang,Junichi Sadoshima,Stephen F Vatner,Dorothy E Vatner,

We examined the role of p38alpha MAPK in mediating cardiomyopathy in mice overexpressing beta(1)-adrenergic receptor (beta(1)-AR) or beta(2)-AR by mating them with dominant-negative p38alpha (DNp38alpha) MAPK mice. Both beta(1)-AR and beta(2)-AR Tg mice had enhanced LV ejection fraction (LVEF) as young adults and developed similar cardiomyopathy at 11-15 months, characterized by reduced LVEF, myocyte hypertrophy, fibrosis, and apoptosis. We inhibited p38alpha MAPK by mating beta(1)-AR Tg and beta(2)-AR Tg mice with DNp38alpha MAPK mice, which rescued the depressed LVEF and reduced apoptosis and fibrosis in bigenic beta(2)-AR x DNp38alpha MAPK mice, but not bigenic beta(1)-AR x DNp38alpha MAPK mice, and failed to reduce myocyte hypertrophy in either group. G(salpha) was increased in both beta(1)-AR Tg and beta(2)-AR Tg mice and was still present in bigenic beta(1)-AR x DNp38alpha MAPK mice, but not bigenic beta(2)-AR x DNp38alpha MAPK mice. This suggests that p38alpha MAPK is one critical downstream signal for the development of cardiomyopathy following chronic beta(2)-AR stimulation, but other kinases may be more important in ameliorating the adverse effects of chronic beta(1)-AR stimulation.

Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Publishing Authors By Initials

PS Peter,JE Brady,L Yan,W Chen,S Engelhardt,Y Wang,J Sadoshima,SF Vatner,DE Vatner,

For similar proteins: membrane proteins: receptors, cell surface: receptors, biogenic amine: receptors, catecholamine: receptors, adrenergic: receptors, adrenergic, beta: receptors, adrenergic, beta-2 research abstracts see: proteins: membrane proteins: receptors, cell surface: receptors, biogenic amine: receptors, catecholamine: receptors, adrenergic: receptors, adrenergic, beta: receptors, adrenergic, beta-2 research

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Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of clinical investigation

VOLUME: 117

Page Numbers: 1335-43

Journal Abbreviation:

ISSN: 0021-9738

DAY: 19

MONTH: 04

YEAR: 2007

Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7802877

Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Keywords Mesh Terms:

KEYWORDS: Receptors, Adrenergic, beta-2

MESH TERMS: physiology

Chemical & Substance for Abstract: Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor. Information

Substance Name: Mitogen-Activated Protein Kinase 14

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Inhibition of p38 alpha MAPK rescues cardiomyopathy induced by overexpressed beta 2-adrenergic receptor, but not beta 1-adrenergic receptor.

AFFILIATION: Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL 69752

ACRONYM: HL

MEDLINETA: J Clin Invest

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