| Texto completo | |
| Autor(es): |
Malvestio, Lygia M.
;
Celes, Mara Rubia N.
;
Jelicks, Linda A.
;
Tanowitz, Herbert B.
;
Prado, Cibele M.
Número total de Autores: 5
|
| Tipo de documento: | Artigo Científico |
| Fonte: | Parasitology Research; v. 116, n. 1, p. 5-pg., 2017-01-01. |
| Resumo | |
Dystrophin, an important protein of the dystrophin-glycoprotein complex, has been implicated in the pathogenesis of experimental Chagas disease. It is important for the maintenance of cell shape and contraction force transmission. Dystrophin loss has been related to end-stage cardiac myopathies and proposed as a common route for myocardial dysfunction and progression to advanced heart failure. Evidence suggests that calpains, calcium-dependent proteases, digest dystrophin when the calcium concentration is compatible with their activation. The objective of this in vitro study was to test the hypothesis that dantrolene, a calcium channel blocker, improves structural changes induced by serum from Trypanosoma cruzi-infected mice. Cultured neonatal cardiac myocytes were incubated with serum from T. cruzi-infected mice and treated with dantrolene for 24 h. Immunofluorescence and immunoblotting were performed to evaluate dystrophin and calpain-1 protein expression. The levels of dystrophin decreased 13% and calpain increased 17% after incubation of cultured neonatal cardiac myocytes with serum from T. cruzi-infected mice. The treatment with dantrolene restored the dystrophin and calpain levels near control levels. Our results demonstrate that alterations in calcium homeostasis in cardiac myocytes are responsible, in part, for cardiac structural changes in experimentally induced T. cruzi myocarditis and that calpain inhibitors may be beneficial in Chagasic heart disease. (AU) | |
| Processo FAPESP: | 09/17787-8 - Hipertensão arterial, hipertrofia e falência cardíaca e complexo de glicoproteínas associadas à distrofina. |
| Beneficiário: | Cibele Maria Prado Zinni |
| Modalidade de apoio: | Auxílio à Pesquisa - Jovens Pesquisadores |
| Processo FAPESP: | 09/53544-2 - Avaliação in vitro da expressão de distrofina em cardiomiócitos submetidos a diferentes estímulos |
| Beneficiário: | Marcos Antonio Rossi |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 10/19216-5 - Hipertensão arterial, hipertrofia e falência cardíaca e complexo de glicoproteínas associadas à distrofina |
| Beneficiário: | Cibele Maria Prado Zinni |
| Modalidade de apoio: | Bolsas no Brasil - Jovens Pesquisadores |
| Processo FAPESP: | 10/18629-4 - O papel do cálcio, da calpaína, de citocinas pró-inflamatórias e de hipóxia na expressão de distrofina em cardiomiócitos: estudo in vitro |
| Beneficiário: | Lygia Maria Mouri Malvestio |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado Direto |