J Korean Soc Pediatr Nephrol.
2011 Apr;15(1):38-48. 10.3339/jkspn.2011.15.1.38.
Transcriptome Profiling of Kidney Tissue from FGS/kist Mice, the Korean Animal Model of Focal Segmental Glomerulosclerosis
- Affiliations
-
- 1Department of Pediatrics, Seoul National University Children's Hospital, Seoul, South Korea. cheonghi@snu.ac.kr
- 2Department of Pediatrics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
- 3Animal Model Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Yusong, South Korea.
- 4Kidney Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul, South Korea.
- 5Department of Pediatrics, Inje University Haeundae Paik Hospital, Busan, South Korea.
- KMID: 1442144
- DOI: http://doi.org/10.3339/jkspn.2011.15.1.38
Abstract
- PURPOSE
Focal segmental glomerulosclerosis (FSGS) is the most common glomerulopathy causing pediatric renal failure. Since specific treatment targeting the etiology and pathophysiology of primary FSGS is yet elusive, the authors explored the pathophysiology of FSGS by transcriptome analysis of the disease using an animal model.
METHODS
FGS/kist strain, a mouse model of primary FSGS, and RFM/kist strain, as control and the parent strain of FGS/kist, were used. Kidney tissues were harvested and isolated renal cortex was used to extract mRNA, which was run on AB 1700 mouse microarray chip after reverse transcription to get the transcriptome profile.
RESULTS
Sixty two genes were differentially expressed in FGS/kist kidney tissue compared to the control. Those genes were related to cell cycle/cell death, immune reaction, and lipid metabolism/vasculopathy, and the key molecules of their networks were TNF, IL-6/4, IFNgamma, TP53, and PPARgamma.
CONCLUSION
This study confirmed that renal cell death, immune system activation with subsequent fibrosis, and lipid metabolism-related early vasculopathy were involved in the pathophysiology of FSGS. In addition, the relevance of methodology used in this study, namely transcriptome profiling, and Korean animal model of FGS/kist was validated. Further study would reveal novel pathophysiology of FSGS for new therapeutic targets.
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