Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction.

Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Research Abstract Details 

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Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Abstract Text:

Marina R Bergman,John R Teerlink,Rajeev Mahimkar,Luyi Li,Bo-Qing Zhu,Anita Nguyen,Sia Dahi,Joel S Karliner,David H Lovett,

Although enhanced cardiac matrix metalloproteinase (MMP)-2 synthesis has been associated with ventricular remodeling and failure, whether MMP-2 expression is a direct mediator of this process is unknown. We generated transgenic mice expressing active MMP-2 driven by the alpha-myosin heavy chain promoter. At 4 mo MMP-2 transgenic hearts demonstrated expression of the MMP-2 transgene, myocyte hypertrophy, breakdown of Z-band registration, lysis of myofilaments, disruption of sarcomere and mitochondrial architecture, and cardiac fibroblast proliferation. Hearts from 8-mo-old transgenic mice displayed extensive myocyte disorganization and dropout with replacement fibrosis and perivascular fibrosis. Older transgenic mice also exhibited a massive increase in cardiac MMP-2 expression, representing recruitment of endogenous MMP-2 synthesis, with associated expression of MMP-9 and membrane type 1 MMP. Increases in diastolic [control (C) 33 +/- 3 vs. MMP 51 +/- 12 microl; P = 0.003] and systolic (C 7 +/- 2 vs. MMP 28 +/- 14 microl; P = 0.003) left ventricular (LV) volumes and relatively preserved stroke volume (C 26 +/- 4 vs. MMP 23 +/- 3 microl; P = 0.16) resulted in markedly decreased LV ejection fraction (C 78 +/- 7% vs. MMP 48 +/- 16%; P = 0.0006). Markedly impaired systolic function in the MMP transgenic mice was demonstrated in the reduced preload-adjusted maximal power (C 240 +/- 84 vs. MMP 78 +/- 49 mW/microl(2); P = 0.0003) and decreased end-systolic pressure-volume relation (C 7.5 +/- 1.5 vs. MMP 4.7 +/- 2.0; P = 0.016). Expression of active MMP-2 is sufficient to induce severe ventricular remodeling and systolic dysfunction in the absence of superimposed injury.

Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Publishing Authors By Initials

MR Bergman,JR Teerlink,R Mahimkar,L Li,BQ Zhu,A Nguyen,S Dahi,JS Karliner,DH Lovett,

For similar circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: ventricular function: ventricular remodeling research abstracts see: circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: ventricular function: ventricular remodeling research

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MEDLINE DATE:

Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Journal Published:

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

Journal: American journal of physiology. Heart and circulat

VOLUME: 292

Page Numbers: H1847-60

Journal Abbreviation:

ISSN: 0363-6135

DAY: 8

MONTH: 12

YEAR: 2006

Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Keywords Mesh Terms:

KEYWORDS: Ventricular Remodeling

MESH TERMS: physiology

Chemical & Substance for Abstract: Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Information

Substance Name: Matrix Metalloproteinase 14

Registry Number: EC 3.4.24.80

Grant and Affiliation Information for Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction.

AFFILIATION: Department of Medicine, San Francisco Department of Veterans Affairs Medical Center/University of California, San Francisco, California 94121, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: P01-HL-68738

ACRONYM: HL

MEDLINETA: Am J Physiol Heart Circ Physio

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