S100B expression modulates left ventricular remodeling after myocardial infarction in mice.

Abstract:

BACKGROUND: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 hypertrophy after infarction. METHODS AND RESULTS:We compared 21 wild-type (WT), 20 TG, and 24 KO mice over 35 days after experimental myocardial infarction with sham-operated controls (n=56). Of those, 4 WT-infarcted mice, 7 TG-infarcted mice, and 1 KO-infarcted mouse and no sham-operated mice died during the observation period. Among survivors, echocardiography, hemodynamic studies, and postmortem examination indicated that the WT and KO groups of infarcted mice mounted a hypertrophic response that was augmented in KO mice. The S100B-overexpressing TG group did not develop hypertrophy but demonstrated increased apoptosis. The postinfarct end-diastolic pressure was lower in KO mice than in WT mice, in accordance with other structural, hemodynamic, and functional parameters, which suggests that abrogation of S100B expression augmented hypertrophy, decreased apoptosis, and was beneficial to preservation of cardiac function within this time frame. CONCLUSIONS:S100B regulates the hypertrophic response and remodeling in the early postinfarct period and represents a potential novel therapeutic target.

journal_name

Circulation

journal_title

Circulation

authors

Tsoporis JN,Marks A,Haddad A,Dawood F,Liu PP,Parker TG

doi

10.1161/01.CIR.0000154554.65287.F5

subject

Has Abstract

pub_date

2005-02-08 00:00:00

pages

598-606

issue

5

eissn

0009-7322

issn

1524-4539

pii

111/5/598

journal_volume

111

pub_type

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