| Texto completo | |
| Autor(es): |
Prado, Fernanda P.
[1]
;
dos Santos, Daniele O.
[1]
;
Blefari, Valdecir
[1]
;
Silva, Carlos A.
[2]
;
Machado, Juliano
[3]
;
Kettelhut, Isis do Carmo
[3]
;
Ramos, Simone G.
[1]
;
Baruffi, Marcelo Dias
[4]
;
Salgado, Helio C.
[2]
;
Prado, Cibele M.
[1]
Número total de Autores: 10
|
| Afiliação do(s) autor(es): | [1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pathol, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Phisiol, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Biochem Immunol, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Pharmaceut Sci Ribeirao Preto, Dept Clin Anal Toxicol & Food Sci, Ribeirao Preto, SP - Brazil
Número total de Afiliações: 4
|
| Tipo de documento: | Artigo Científico |
| Fonte: | PLoS One; v. 12, n. 12 DEC 21 2017. |
| Citações Web of Science: | 2 |
| Resumo | |
Hypertension causes cardiac hypertrophy, one of the most important risk factors for heart failure (HF). Despite the importance of cardiac hypertrophy as a risk factor for the development of HF, not all hypertrophied hearts will ultimately fail. Alterations of cytoskeletal and sarcolemma-associated proteins are considered markers cardiac remodeling during HF. Dystrophin provides mechanical stability to the plasma membrane through its interactions with the actin cytoskeleton and, indirectly, to extracellular matrix proteins. This study was undertaken to evaluate dystrophin and calpain-1 in the transition from compensated cardiac hypertrophy to HF. Wistar rats were subjected to abdominal aorta constriction and killed at 30, 60 and 90 days post surgery (dps). Cardiac function and blood pressure were evaluated. The hearts were collected and Western blotting and immunofluorescence performed for dystrophin, calpain-1, alpha-fodrin and calpastatin. Statistical analyses were performed and considered significant when p<0.05. After 90 dps, 70% of the animals showed hypertrophic hearts (HH) and 30% hypertrophic+dilated hearts (HD). Systolic and diastolic functions were preserved at 30 and 60 dps, however, decreased in the HD group. Blood pressure, cardiomyocyte diameter and collagen content were increased at all time points. Dystrophin expression was lightly increased at 30 and 60 dps and HH group. HD group showed decreased expression of dystrophin and calpastatin and increased expression of calpain-1 and alpha-fodrin fragments. The first signals of dystrophin reduction were observed as early as 60 dps. In conclusion, some hearts present a distinct molecular pattern at an early stage of the disease; this pattern could provide an opportunity to identify these failure-prone hearts during the development of the cardiac disease. We showed that decreased expression of dystrophin and increased expression of calpains are coincident and could work as possible therapeutic targets to prevent heart failure as a consequence of cardiac hypertrophy. (AU) | |
| Processo FAPESP: | 12/23649-0 - Cardiomiopatia séptica como componente da síndrome de falência de múltiplos órgãos na sépsis grave |
| Beneficiário: | Simone Gusmão Ramos |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 16/21710-4 - Determinação do padrão de resposta imunológica (Th1, Th2 e/ou Th17) predominante na fase inicial e tardia do desenvolvimento de aneurisma de aorta abdominal em ratos Wistar associado ao consumo de dieta hipercolesterolêmica |
| Beneficiário: | Simone Gusmão Ramos |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| 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: | 13/20549-7 - Avanços na regulação cardiocirculatória em condições fisiológica e fisiopatológica |
| Beneficiário: | Helio Cesar Salgado |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| 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: | 15/21112-7 - CONTROLE DA MASSA MUSCULAR PELA VIA DE SINALIZAÇÃO DO AMPc |
| Beneficiário: | Juliano Machado |
| Modalidade de apoio: | Bolsas no Brasil - Pós-Doutorado |
| Processo FAPESP: | 09/54010-1 - EMU: sepsis e choque séptico: alterações funcionais e morfológicas do coração. Estudo experimental em camundongos |
| Beneficiário: | Helio Cesar Salgado |
| Modalidade de apoio: | Auxílio à Pesquisa - Programa Equipamentos Multiusuários |