Renal ischemia/reperfusion-induced cardiac hypertrophy in mice: Cardiac morphological and morphometric characterization

Autor(es)

Cirino-Silva, Rogerio ; Kmit, Fernanda V. ; Trentin-Sonoda, Mayra ; Nakama, Karina K. ; Panico, Karine ; Alvim, Juliana M. ; Dreyer, Thiago R. ; Martinho-Silva, Herculano ; Carneiro-Ramos, Marcela S.

• Tipo de documento: Artigo Científico
• Fonte: JRSM CARDIOVASCULAR DISEASE; v. 6, JAN 1 2017.
• Citações Web of Science: 0

Resumo

Background: Tissue remodeling is usually dependent on the deposition of extracellular matrix that may result in tissue stiffness and impaired myocardium contraction. Objectives: We had previously demonstrated that renal ischemia/reperfusion (I/R) is able to induce development of cardiac hypertrophy in mice. Therefore, we aimed to characterize renal I/R-induced cardiac hypertrophy. Design: C57BL/6J mice were subjected to 60 minutes' unilateral renal pedicle occlusion, followed by reperfusion (I/R) for 5, 8, 12 or 15 days. Gene expression, protein abundance and morphometric analyses were performed in all time points. Results: Left ventricle wall thickening was increased after eight days of reperfusion (p<0.05). An increase in the number of heart ventricle capillaries and diameter after 12 days of reperfusion (p<0.05) was observed; an increase in the density of capillaries starting at 5 days of reperfusion (p<0.05) was also observed. Analyses of MMP2 protein levels showed an increase at 15 days compared to sham (p<0.05). Moreover, TGF-beta gene expression was downregulated at 12 days as well TIMP 1 and 2 (p<0.05). The Fourier-transform infrared spectroscopy analysis showed that collagen content was altered only in the internal section of the heart (p<0.05); such data were supported by collagen mRNA levels. Conclusions: Renal I/R leads to impactful changes in heart morphology, accompanied by an increase in microvasculature. Although it is clear that I/R is able to induce cardiac remodeling, such morphological changes is present in only a section of the heart tissue. (AU)

• Processo FAPESP: 15/19107-5 - TLR4 e sistema complemento: possível mecanismo chave na resposta hipertrófica do tecido cardíaco em quadro inflamatório sistêmico induzido por lesão isquêmica renal
• Beneficiário: Marcela Sorelli Carneiro Ramos
• Modalidade de apoio: Auxílio à Pesquisa - Regular