Intercalated Disc and Dystrophin-Glycoprotein Complex Remodeling in the Hearts of Mice Submitted to Severe Sepsis

Author(s):	Celes, M. R. N. ; Torres-Duenas, D. ; Campos, E. C. ; Prado, C. M. ; Cunha, F. Q. ; Rossi, M. A. ; Kimchi, A Total Authors: 7
Document type:	Journal article
Source:	CURRENT ADVANCES IN HEART DISEASE; v. N/A, p. 2-pg., 2008-01-01.
Abstract
Impairment of myocardial contractility in severe sepsis/septic shock in the absence of preload and afterload has been recognized as an important factor that contributes to the high mortality in critically-ill patients Evidence from our laboratory indicates that myocardial structural changes could be responsible for sepsis-induced myocardial dysfunction. This study was tests the hypotheses that alterations in Intercellular communication and mechanical coupling between neighboring cardiomyocytes and in dystrophin-glycoprotein complex (DGC) could occur in severe experimental sepsis and contribute to myocardial depression. Male C57BI/6 mice were subjected to moderate (MSI) or severe (SSI) septic injury induced by cecal ligation and puncture (CLP). Our results showed a decreased expression of gap (connexin43) and adherens junction (N-cadherin) proteins with remodeling of the intercalated disc in severe sepsis. In addition, there was a decreased expression of major proteins, dystrophin and beta-dystroglican, implicated in the mechanical binding between the entire arrays of myofibrils to the extracellular matrix. It is our interpretation that these changes could contribute to myocardial depression in sepsis. (AU)