Advanced search
Start date
Betweenand
Related content
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Early dystrophin loss is coincident with the transition of compensated cardiac hypertrophy to heart failure

Full text
Author(s):
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]
Total Authors: 10
Affiliation:
[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
Total Affiliations: 4
Document type: Journal article
Source: PLoS One; v. 12, n. 12 DEC 21 2017.
Web of Science Citations: 2
Abstract

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)

FAPESP's process: 12/23649-0 - Septic cardiomyophaty as a component of multiple organ dysfunction syndrome in severe sepsis
Grantee:Simone Gusmão Ramos
Support Opportunities: Regular Research Grants
FAPESP's process: 16/21710-4 - Determination of the pattern of immune response(Th1, Th2 and/or Th17) predominant in early and late development of abdominal aortic aneurysm in Wistar rats associated with hypercholesterolemic diet consumption
Grantee:Simone Gusmão Ramos
Support Opportunities: Regular Research Grants
FAPESP's process: 09/17787-8 - High blood pressure, cardiac hypertrophy, heart failure and dystrophin-glycoprotein complex
Grantee:Cibele Maria Prado Zinni
Support Opportunities: Research Grants - Young Investigators Grants
FAPESP's process: 13/20549-7 - New insights in cardiovascular regulation under physiological and pathophysiological condition
Grantee:Helio Cesar Salgado
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 10/19216-5 - Hypertension, cardiac hypertrophy and cardiac failure and dystrophin glycoproteins
Grantee:Cibele Maria Prado Zinni
Support Opportunities: Scholarships in Brazil - Young Researchers
FAPESP's process: 09/54010-1 - Sepsis and septic shock: functional and morphological changes in the heart. An experimental study in mice
Grantee:Helio Cesar Salgado
Support Opportunities: Multi-user Equipment Program