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

Autor(es)

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]

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: Experimental and Molecular Pathology; v. 100, n. 1, p. 167-176, FEB 2016.
• Citações Web of Science: 6

Resumo

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)

• 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: 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: 12/09665-2 - Hipertensão arterial, hipertrofia e falência cardíaca e complexo de glicoproteínas associadas à distrofina
• Beneficiário: Rubens Fernando Pedro
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• 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
• Processo FAPESP: 14/07527-7 - O papel do TGF-B na evolução da hipertrofia compensada para hipertrofia descompensada em ratos submetidos à estenose de aorta abdominal
• Beneficiário: Thayane Rafaela Feola Pizzo
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 11/08855-0 - Hipertensão arterial, hipertrofia e falência cardíaca e complexo de glicoproteínas associadas à distrofina.
• Beneficiário: Mayara Segundo Ribeiro
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica