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논문분류	춘계학술대회 초록집
제목	Autophagy in FOXD1 stroma-derived cells plays a critical role in renal tubulointerstitial fibrosis
저자	Sun ah NAM2, Wan-young KIM2, Sang hee PARK3, Hong lim KIM4, Chul woo YANG1, Jin KIM2, *Yong kyun KIM1
출판정보	2017; 2017(1):
키워드	autophagy, kidney, fibrosis, apoptosis
초록	Objectives : Renal fibrosis is the final common pathway of various renal injuries and it leads to chronic kidney disease. FOXD1+ progenitors give rise to an extensive population of stromal cell, which mature to form vascular smooth cell, glomerular mesangial cells and pericytes. FOXD1 lineage pericyte plays a critical role in renal tubulointerstitial fibrosis (TIF). Autophagy is a cellular process of degradation of damaged cytoplasmic components and regulates cell death and proliferation. In this study, we investigated the role of autophagy in FOXD1 stroma-derived cells on renal TIF using conditional knockout mice in which Atg7 was genetically ablated specifically in FOXD1 stroma-derived cells. Methods : We generated conditional knockout mice in which Atg7 is genetically ablated specifically in FOXD1-cells (Atg7flox/flox;FOXD1-Cre+) and performed unilateral ureteral obstruction (UUO). Atg7flox/flox litermates served as controls. Results : Extracellular matrix deposition and the protein expression of TGF-β and α-smooth muscle antibody were substantially increased in the obstructed kidneys of Atg7flox/flox;FOXD1-Cre+ mice after UUO with those of WT mice. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay revealed that the number of TUNEL-positive cells was significantly greater in obstructed kidneys of in Atg7flox/flox;FOXD1-Cre+ compared with WT mice after UUO. TUNEL-positive cells were co-localized with PDGFR-β and tubular cell markers. The protein expression of C-myc was substantially increased in the obstructed kidneys of Atg7flox/flox;FOXD1-Cre+ mice. Conclusions : Our data showed that autophagy in FOXD1 stroma-derived cells play a protective role in development of renal TIF and apoptosis of stromal cell as well as tubular epithelial cells, which may be a new therapeutic target for renal TIF.
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