| 국소성 분절성 사구체 신병증의 동물 모델 (FGS/kist 생쥐) 신 조직의 유전자 발현 양상 |
| 강희경, 이병섭, 이철호, 하일수, 정해일, 최용 |
1서울대학교병원 소아청소년과
2울산대학교 의과대학 소아청소년과
3한국생명공학연구원
4서울대학교병원 소아청소년과
5서울대학교병원 소아청소년과
6인제대학교 부산해운대백병원 소아청소년과 |
| Transcriptome Profiling of Kidney Tissue from FGS/kist Mice, the Korean Animal Model of Focal Segmental Glomerulosclerosis |
| Hee-Gyung Kang, Byong-Sop Lee, Chul-Ho Lee, Il-Soo Ha, Hae-Il Cheong, Yong Choi |
1Department of Pediatrics, Seoul National University Children's Hospital
2Department of Pediatrics, Asan Medical Center, University of Ulsan College of Medicine
3Animal Model Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
4Department of Pediatrics, Seoul National University Children's Hospital
5Department of Pediatrics, Seoul National University Children's Hospital
6Department of Pediatrics, Inje University Haeundae Paik Hospital |
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Received: March 19, 2011; Accepted: April 15, 2011. |
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| ABSTRACT |
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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. |
| Key words:
Focal segmental glomerulosclerosis | Transcriptome | Laboratory Animal Models |
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