Time Course of Gene Expression Profile in Renal Ischemia and Reperfusion Injury in Mice

Transplant Proc. 2020 Dec;52(10):2970-2976. doi: 10.1016/j.transproceed.2020.06.029. Epub 2020 Aug 3.

Abstract

Ischemic renal failure is an inflammatory disease that can affect various organs, including the heart. The organ responds to the stimulus and undergoes tissue remodeling that can result in cardiac hypertrophy. This study aimed to characterize the cardiac global gene expression profile in renal ischemia/reperfusion (IR) model using microarray technology. To do that, left kidney ischemia was induced in male C57BL/6 mice for 60 minutes, followed by reperfusion (IR) for 5, 8, 15, or 20 days post ischemia (dpi). Total cardiac tissue RNA was extracted and hybridized to chips with 35,000 mouse genes. The GeneChip Mouse Genome 430 2.0 Array Expression chip (Affymetrix) was used, and CEL files generated were processed with DNA-Chip-Analyzer (dCHIP) software. Subsequent analysis considered only differences among groups of at least 1.2-fold (up or down) expression changes. Analyses of the samples indicated positive modulation of 17,413 genes and 405 pathways and negative modulation of 18,287 genes and 300 pathways. A narrower analysis of genes related to inflammation, metabolism, apoptosis, oxidative stress, and channels/ion transport was performance, and it was correlated with IR injury, corroborating previous data from literature. Renal IR induced a global shift in cardiac tissue gene expression; in particular, genes related to the inflammatory system and cardiomyocyte function were changed. The in-depth study of the cell signaling in the present study could stimulate the development of new therapeutic option to ameliorate the outcome of renal-IR-induced heart damage.

MeSH terms

  • Acute Kidney Injury / complications
  • Acute Kidney Injury / metabolism
  • Animals
  • Cardiomegaly / etiology*
  • Cardiomegaly / genetics*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Myocytes, Cardiac / metabolism
  • Reperfusion Injury / complications*
  • Reperfusion Injury / genetics
  • Reperfusion Injury / metabolism
  • Transcriptome