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GLOBAL GENE EXPRESSION PROFILE IN RENAL ISCHEMIA/REPERFUSION INDUCED CARDIAC HYPERTROPHY
Author(s) -
Nakama Karina Kaori,
Carneiro-Ramos Marcela Sorelli
Publication year - 2012
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.26.1_supplement.1134.13
Subject(s) - inflammation , ischemia , gene expression , medicine , muscle hypertrophy , gene , kidney , immune system , heart failure , reperfusion injury , real time polymerase chain reaction , biology , immunology , genetics
Objectives The heart is a target organ in many regulatory systems, such as hormones, neuronal and immunological systems, modulating heart trophism. This study aimed to determine changes in gene expression of hypertrophied cardiac tissue in a renal ischemia‐induced systemic inflammation model. Methods C57BL/6 mice were submitted to unilateral occlusion of left renal pedicle for 60 min, followed by reperfusion of 5, 8, 15 and 20 days. The software dChip and GeneMAPP were used to separate and group genes in signaling pathways which had shown significant increase or decrease in expression. Three genes (H2‐Oa, Crtam and Ifnz) of very modulated pathways associated with immune response (MHC class II, Positive Regulation of Natural Killer Cell and Cytokine Activity Pathways, respectively) were selected. To validate array results, real time PCR was performed. Results The analysis results indicated 17,413 up‐regulated and 18,297 down‐regulated genes, and 405 up‐regulated and 300 down‐regulated pathways. According to the array analysis and real time PCR results the three selected genes were up regulated and showed a greater increase after 8 days of reperfusion. Conclusion Validation of H2‐Oa, Crtam and Ifnz indicates a possible relationship of these genes in the development of cardiac hypertrophy due to a systemic condition of inflammation caused by renal failure.