Transcriptome Profiling of Kidney Tissue from FGS/kist Mice, the Korean Animal Model of Focal Segmental Glomerulosclerosis

Kang, Hee-Gyung; Lee, Byong-Sop; Lee, Chul-Ho; Ha, Il-Soo; Cheong, Hae-Il; Choi, Yong

doi:2011.15.1.38

J Korean Soc Pediatr Nephrol > Volume 15(1); 2011 > Article

J Korean Soc Pediatr Nephrol 2011;15(1): 38-48. doi: https://doi.org/10.3339/jkspn.2011.15.1.38

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

Received: March 19, 2011; Accepted: April 15, 2011.

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, IFN${gamma}$, TP53, and PPAR${gamma}$.
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