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TOLL‐LIKE RECEPTOR 2 IS INCREASED IN RENAL ISCHEMIA/REPERFUSION‐INDUCED CARDIAC HYPERTROPHY IN MICE
Author(s) -
Sonoda Mayra Trentin,
Silva Rogerio Cirino,
CarneiroRamos Marcela Sorelli
Publication year - 2011
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.25.1_supplement.lb457
Subject(s) - medicine , endocrinology , tlr2 , kidney , muscle hypertrophy , receptor , renal ischemia , ischemia , tlr4 , cardiac hypertrophy , reperfusion injury
Objectives The innate immune response can exerts innumerous effects in vast number of tissues and organs. It's well established that cytokines and Toll‐like receptors (TLRs) participate of cardiac trophism modulation. The aim of this study was to investigate the role of TLRs in heart after renal ischemia/reperfusion. Methods C57bl/6J mice were subjected to unilateral 60 minutes kidney ischemia, followed by reperfusion of 5, 8, 15 and 20 days. Levels of urea were measured to confirm renal failure and gene expression were analyzed by real time PCR. 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 (p<0.05) and ANF mRNA levels (p<0.001), a cardiac hypertrophy marker, when compared to sham group. Cardiac TLR‐2 mRNA levels was increased after 5 days of reperfusion (p<0.05) when compared to sham group. The isoform TLR‐4 has a tendency to increase, but it was not significant. Conclusion First, the results indicate that renal ischemia/reperfusion model is able to induce a transient cardiac hypertrophy in mice. Moreover, this hypertrophy has a positive correlation with a transient increase of TLR2 mRNA levels, suggesting that the cascade of activation of TLRs may be involved to cardiac hypertrophy development. Financial Support: FAPESP, CNPq.