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1 Systems Biology, Texas A&M Health Science Center, Collge Station, Texas, United States
2 Systems Biology, Texas A&M Health Science Center, College Station, Texas, United States
3 Systems Biology and Translational Medicine, College of Medicine Texas A&M Health Science Center, College Station, Texas, United States
4 Veterinary Integrated Biosciences, College of Veterinary Medicine Texas A&M University, College Station, Texas, United States
5 Medicine-Renal, Harvard Medical School, Boston, Massachusetts, United States
6 Harvard Institutes of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, United States
7 Systems Biology, Texas A&M Health Science Center, Collge Station, Texas, United States; Medical Physiology, Texas A&M University Health Science Center, College Station, Texas, United States
8 Department of Vet. Anatomy and Public Health, Texas A&M University College of Vet Medicine, College Station, Texas, United States; Veterinary Integrated Biosciences, College of Veterinary Medicine Texas A&M Health Science Center, College Station, Texas, United States
9 Systems Biology, Texas A&M Health Science Ctr, College Station, Texas, United States
* To whom correspondence should be addressed. E-mail: parrish{at}medicine.tamhsc.edu.
Aging is associated with an increased incidence and severity of acute renal failure. However, the molecular mechanism underlying the increased susceptibility to injury remain undefined. These experiments were designed to investigate the response of aged kidney to ischemic injury and to identify candidate genes that may mediate this response. Renal slices prepared from young (5 month), aged ad libitum (aged-AL; 24 month) and aged caloric restricted (aged-CR; 24 month) male Fischer 344 rats were subjected to ischemic stress (100% N2) for 0-60 min. As assessed by biochemical and histological evaluation, slices from aged-AL rats were more susceptible to injury than young counterparts and this was attenuated by caloric restriction. In an attempt to identify the molecular pathway(s) underlying this response, RNA was isolated and the corresponding cDNA was hybridized to CodeLink Rat Whole Genome Bioarray slides. Subsequent gene expression analysis was performed using GeneSpring software. Using two-sample t-tests and a 2-fold cut-off, the expression of 92 genes was changed during aging and attenuated by caloric restriction, including claudin-7, Kim-1 and MMP-7. Claudin-7 gene expression peaked at 18 months, however increased protein expression in certain tubular epithelial cells was seen at 24 months. Kim-1 gene expression was not elevated at 8 or 12 months, but was at 18 and 24 months. Increased Kim-1 protein expression was only seen at 24 months and corresponded to increased urinary levels. MMP-7 gene expression was decreased at 8 months, but an age-dependent increase was seen at 24 months and correlated with the gene expression pattern.
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