S100B expression modulates left ventricular remodeling after myocardial infarction in mice

S100B, a 20-kDa, Ca2+-binding dimer, is a putative intrinsic negative regulator of myocardial hypertrophy expressed after myocardial infarction. S100B-overexpressing transgenic (TG) and S100B-knockout (KO) mice have been generated to assess the consequences of S100B expression and altered hypertroph...

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Veröffentlicht in:	Circulation (New York, N.Y.) N.Y.), 2005-02, Vol.111 (5), p.598-606
Hauptverfasser:	TSOPORIS, James N, MARKS, Alexander, HADDAD, Abraham, DAWOOD, Fayez, LIU, Peter P, PARKER, Thomas G
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Coronary heart disease Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Gene Expression Heart Heart - embryology Heart Ventricles - pathology Hypertrophy, Left Ventricular - pathology Medical sciences Mice Mice, Knockout Mice, Transgenic Myocardial Infarction - diagnostic imaging Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium - metabolism Myocytes, Cardiac - pathology Nerve Growth Factors - genetics Nerve Growth Factors - metabolism Neurology Protein Biosynthesis S100 Calcium Binding Protein beta Subunit S100 Proteins - genetics S100 Proteins - metabolism Survival Analysis Ultrasonography Vascular diseases and vascular malformations of the nervous system Ventricular Function, Left Ventricular Remodeling
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