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Are adherens junctions implicated in the transition from physiological to pathological cardiac hypertrophy?
Author(s) -
Prado Cibele M,
Blefari Valdecir,
Santos Daniele O.,
Malvestio Lygia MM,
Pedro Rubens F.,
Rossi Marcos M.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.745.6
Subject(s) - adherens junction , medicine , cardiology , pathogenesis , muscle hypertrophy , heart failure , ejection fraction , stenosis , abdominal aorta , aorta , chemistry , cadherin , cell , biochemistry
Hypertension causes cardiac hypertrophy, cardiac dysfunction, and heart failure (HF). The mechanisms implicated in the transition from physiological to pathological hypertrophy are still unknown. Growing evidence points out to the role of inappropriate mechanical coupling in the pathogenesis of HF. We investigated adherens junctions and its potential role in the pathogenesis of HF in rats submitted to chronic abdominal aorta stenosis. Wistar rats were submitted to abdominal aorta stenosis and killed at 90 days post surgery: 60% presented hypertrophied hearts (HH) and 40% hypertrophied and dilated hearts (DH), as evaluated by echocardiography. DH and HH were compared to control hearts. The hearts were collected and Western blot (WB) and immunofluorescence (IF) were performed for cadherin, beta‐catenin and calpain. Blood pressure was evaluated. Data were considered significant when p<0.05. Cadherin reduced 20% in HH and 64% in DH; beta‐catenin reduced 32% in DH and calpain increased 50% in DH as compared to control. The ejection fraction reduced 35% in DH. Adherens junctions remodeling may be partly responsible for the development of heart failure in rats submitted to chronic abdominal aorta stenosis. These abnormal parameters may emerge as therapeutic targets to modulate the evolution of heart hypertrophy from compensated to decompensated phase. Grants from FAPESP 09/17787–8; 09/54010–1; 10/19216–5.