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
Circulationjournal_title
Circulationauthors
Tsoporis JN,Marks A,Haddad A,Dawood F,Liu PP,Parker TGdoi
10.1161/01.CIR.0000154554.65287.F5subject
Has Abstractpub_date
2005-02-08 00:00:00pages
598-606issue
5eissn
0009-7322issn
1524-4539pii
111/5/598journal_volume
111pub_type
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