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

Reduced expression of adherens and gap junction proteins can have a fundamental role in the development of heart failure following cardiac hypertrophy in rats

Full text
Author(s):
dos Santos, Daniele O. [1] ; Blefari, Valdecir [1] ; Prado, Fernanda P. [1] ; Silva, Carlos A. [2] ; Fazan, Jr., Rubens [2] ; Salgado, Helio C. [2] ; Ramos, Simone G. [1] ; Prado, Cibele M. [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pathol, Ave Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Experimental and Molecular Pathology; v. 100, n. 1, p. 167-176, FEB 2016.
Web of Science Citations: 6
Abstract

Hypertension causes cardiac hypertrophy, cardiac dysfunction and heart failure (HF). The mechanisms implicated in the transition from compensated to decompensated cardiac hypertrophy are not fully understood. This study was aimed to investigate whether alterations in the expression of intercalated disk proteins could contribute to the transition of compensated cardiac hypertrophy to dilated heart development that culminates in HF. Male rats were submitted to abdominal aortic constriction and at 90 days post surgery (dps), three groups were observed: sham-operated animals (controls), animals with hypertrophic hearts (HH) and animals with hypertrophic + dilated hearts (HD). Blood pressure was evaluated. The hearts were collected and Western blot and immunofluorescence were performed to desmoglein-2, desmocollin-2, N-cadherin, plakoglobin, B-catenin, and connexin-43. Cardiac systolic function was evaluated using the Vevo 2100 ultrasound system. Data were considered significant when p < 0.05. Seventy percent of the animals presented with HH and 30% were HD at 90 dps. The blood pressure increased in both groups. The amount of desmoglein-2 and desmocollin-2 expression was increased in both groups and no difference was observed in either group. The expression of N-cadherin, plakoglobin and B-catenin increased in the HH group and decreased in the HD group; and connexin-43 decreased only in the HD group. There was no difference between the ejection fraction and fractional shortening at 30 and 60 dps; however, they were decreased in the HD group at 90 dps. We found that while some proteins have increased expression accompanied by the increase in the cell volume associated with preserved systolic cardiac function in the HH group, these same proteins had decreased expression even without significant reduction in the cell volume associated with decreased systolic cardiac function in HD group. The increased expression of desmoglein-2 and desmocollin-2 in both the HH and HD groups could work as a protective compensatory mechanism, helping to maintain the dilated heart. We can hypothesize that inappropriate intercellular mechanical and electrical coupling associated with necrosis and/or apoptosis are important factors contributing to the transition to HF. (C) 2015 Elsevier Inc All rights reserved. (AU)

FAPESP's process: 09/17787-8 - High blood pressure, cardiac hypertrophy, heart failure and dystrophin-glycoprotein complex
Grantee:Cibele Maria Prado Zinni
Support type: Research Grants - Young Investigators Grants
FAPESP's process: 14/07527-7 - The role of TGF-B in the transition of compensated to decompensated heart hypertrophy in rats submitted to abdominal aorta constriction
Grantee:Thayane Rafaela Feola Pizzo
Support type: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 10/19216-5 - Hypertension, cardiac hypertrophy and cardiac failure and dystrophin glycoproteins
Grantee:Cibele Maria Prado Zinni
Support type: Scholarships in Brazil - Young Researchers
FAPESP's process: 12/09665-2 - High blood pressure, cardiac hypertrophy, heart failure and dystrophin glycoprotein complex.
Grantee:Rubens Fernando Pedro
Support type: Scholarships in Brazil - Scientific Initiation
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 type: Multi-user Equipment Program