Title: Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction
Authors: Janssens, Stefan ×
Pokreisz, Peter
Schoonjans, Luc
Pellens, Marijke
Vermeersch, Pieter
Tjwa, Marc
Jans, Peter
Scherrer-Crosbie, M
Picard, MH
Szelid, Z
Gillijns, Hilde
Van de Werf, Frans
Collen, Desire
Bloch, KD #
Issue Date: May-2004
Publisher: Lippincott williams & wilkins
Series Title: Circulation Research vol:94 issue:9 pages:1256-1262
Abstract: Nitric oxide ( NO) is an important modulator of cardiac performance and left ventricular (LV) remodeling after myocardial infarction (MI). We tested the effect of cardiomyocyte-restricted overexpression of one NO synthase isoform, NOS3, on LV remodeling after MI in mice. LV structure and function before and after permanent LAD coronary artery ligation were compared in transgenic mice with cardiomyocyte-restricted NOS3 overexpression (NOS3-TG) and their wild-type littermates (WT). Before MI, systemic hemodynamic measurements, echocardiographic assessment of LV fractional shortening (FS), heart weight, and myocyte width (as assessed histologically) did not differ in NOS3-TG and WT mice. The inotropic response to graded doses of isoproterenol was significantly reduced in NOS3-TG mice. One week after LAD ligation, the infarcted fraction of the LV did not differ in WT and NOS3-TG mice (34 +/- 4% versus 36 +/- 12%, respectively). Four weeks after MI, however, end-systolic LVID was greater, and fractional shortening and maximum and minimum rates of LV pressure development were less in WT than in NOS3-TG mice. LV weight/body weight ratio was greater in WT than in NOS3-TG mice (5.3 +/- 0.2 versus 4.6 +/- 0.5 mg/g; P < 0.01). Myocyte width in noninfarcted myocardium was greater in WT than in NOS3-TG mice (18.8 +/- 2.0 versus 16.6 +/- 1.6 mu m; P < 0.05), whereas fibrosis in noninfarcted myocardium was similar in both genotypes. Cardiomyocyte-restricted overexpression of NOS3 limits LV dysfunction and remodeling after MI, in part by decreasing myocyte hypertrophy in noninfarcted myocardium.
ISSN: 0009-7330
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular and Vascular Biology
Experimental Cardiology
Vesalius Research Centre (-)
Clinical Residents Medicine
× corresponding author
# (joint) last author

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