Isoproterenol Induces Primary Loss of Dystrophin in Rat Hearts: Correlation with Myocardial Injury

Autor(es)

Campos, E. C. ; Romano, M. M. D. ; Celes, M. R. N. ; Prado, C. M. ; Rossi, M. A. ; Kimchi, A

• Tipo de documento: Artigo Científico
• Fonte: CURRENT ADVANCES IN HEART DISEASE; v. N/A, p. 2-pg., 2008-01-01.

Resumo

Alterations in the structural integrity of the sarcolemma of cardiomyocytes have been demonstrated to be caused by isoproterenol. Since sarcolemmal integrity is stabilized by the dystrophin-glycoprotein complex (DGC) that connects actin and laminin in contractile machinery and extracellular matrix and by integrins that also are essential to define cellular-extracellular interaction, this study tests the hypothesis that isoproterenol affects sarcolemmal stability through changes in the DGC and integrins. Immunofluorescent staining revealed that dystrophin is the most sensitive among the structures connecting the actin in the cardiomyocyte cytoskeleton and the extracellular matrix represented by laminin in the present study. The sarcomeric actin dissolution, as part of the process of myocytolysis, occurred after dystrophin reduction or loss. Subsequently, after lysis of myofilaments, the expressions of gamma-sarcoglycan, beta-dystroglycan, beta 1-integrin and laminin alpha-2 were reduced followed by their breakdown, as epiphenomena of the myocytolytic process In conclusion, administration of isoproterenol to rats results in primary loss of dystrophin, the most sensitive among the structural proteins of the DGC. These changes, related to ischemic injury, can explain the severe alterations in the structural integrity of the sarcolemma of cardiomyocytes and hence severe and irreversible injury induced by isoproterenol. (AU)

• Processo FAPESP: 06/59618-0 - O possível papel do complexo de glicoproteínas associadas à distrofia na morte súbita na tripanossomiase americana experimental
• Beneficiário: Marcos Antonio Rossi
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 07/52556-1 - Imunopatogênese da lesão periapical experimentalmente induzida em camundongos knockout de citocinas Th1 (IFNy) e Th2 (IL-4 and IL-10), molécula de adesão intercelular (ICAM-1) e receptor de quimiocina (CCR5): panorama geral de possíveis mecanismos envolvidos no estímulo ou proteção da reabsorção óssea
• Beneficiário: Marcos Antonio Rossi
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 06/52882-3 - O possível papel do complexo de glicoproteínas associadas à distrofina na morte súbita na tripanosomíase americana experimental
• Beneficiário: Cibele Maria Prado Zinni
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 07/59448-0 - O possivel papel do complexo distrofina-glicoproteinas associadas na cardiomiopatia dilatada experimental induzida pelo antineoplasico doxorrubicina.
• Beneficiário: Erica Carolina Campos Pulici
• Modalidade de apoio: Bolsas no Brasil - Doutorado