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RENAL ISCHEMIA REPERFUSION INDUCED CARDIAC HYPERTROPHY: CONTRIBUTION OF EXTRACELLULAR MATRIX ON CARDIAC REMODELING
Author(s) -
Silva Rogerio Cirino,
Sonoda Mayra Trentin,
Ramos Marcela Sorelli Carneiro
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.lb855
Subject(s) - medicine , muscle hypertrophy , cardiac hypertrophy , cardiac function curve , ischemia , extracellular matrix , endocrinology , kidney , blot , renal hypertrophy , cardiology , chemistry , heart failure , biochemistry , diabetic nephropathy , gene
Objectives Cardiac fibroblasts play a crucial role in cardiac function that is directly linked to extracellular matrix production. The focus of this study was to investigate the modulation of the extracellular matrix during cardiac hypertrophy induced by renal ischemic reperfusion. Methods C57bl/6J mice were subjected to unilateral 60 min kidney ischemia, followed by reperfusion of 5, 8, 12, 15 and 20 days. Levels of urea were measured to confirm renal failure, real time PCR, western blotting and FTIR (Fourier Transform Infra Red) were used to molecular analysis. Results Urea levels were increased in groups 5, 15 and 20 days (P<0.05). The group 15 days showed a significant increase in heart weight/body weight ratio when compared to sham group. MMP2 levels showed increased at 12 days of reperfusion (p<0.05), but Collagen levels were not altered in this cardiac hypertrophy model. Conclusion First, the results indicate that renal ischemia/reperfusion model is able to induce a transient cardiac hypertrophy in mice. This hypertrophy was not accompanied to modulation on collagen levels. Financial Support: FAPESP, CNPq and UFABC.