medric medric
[닫기]
잠시만 기다려 주세요. 로딩중입니다.

Tissue-resident natural killer cells exacerbate tubulointerstitial fibrosis by activating transglutaminase 2 and syndecan-4 in a model of aristolochic acid-induced nephropathy

BMB Reports 2019년 52권 9호 p.554 ~ 559
 ( Wee Yu-Mee ) - Asan Medical Center Asan Institute for Life Sciences

 ( Go Heoun-Jeong ) - University of Ulsan College of Medicine Asan Medical Center Department of Pathology
 ( Choi Monica Young ) - Asan Medical Center Asan Institute for Life Sciences
 ( Jung Hey-Rim ) - Asan Medical Center Asan Institute for Life Sciences
 ( Cho Yong-Mee ) - University of Ulsan College of Medicine Asan Medical Center Department of Pathology
 ( Kim Young-Hoon ) - University of Ulsan College of Medicine Asan Medical Center Department of Surgery
 ( Han Duck-Jong ) - University of Ulsan College of Medicine Asan Medical Center Department of Surgery
 ( Shin Sung ) - University of Ulsan College of Medicine Asan Medical Center Department of Surgery

Abstract


Despite reports suggesting that tissue-resident natural killer (trNK) cells cause ischemic kidney injury, their contribution to the development of tubulointerstitial fibrosis has not been determined. This study hypothesized that the depletion of trNK cells may ameliorate renal fibrosis by affecting transglutaminase 2/syndecan-4 interactions. Aristolochic acid nephropathy (AAN) was induced in C57BL/6 mice as an experimental model of kidney fibrosis. The mice were treated with anti-asialo GM1 (ASGM1) or anti-NK1.1 antibodies to deplete NK cells. Although both ASGM1 and NK1.1 antibodies suppressed renal NKp46+DX5+ NK cells, renal NKp46+DX5- cells were resistant to suppression by ASGM1 or NK1.1 antibodies during the development of tubulointerstitial fibrosis in the AAN-induced mouse model. Western blot analysis showed that both antibodies increased the expression of fibronectin, transglutaminase 2, and syndecan-4. These findings indicate that trNK cells played an exacerbating role in tubulointerstitial fibrosis by activating transglutaminase 2 and syndecan-4 in the AAN-induced mouse model.

키워드

Aristolochic acid nephropathy; Syndecan-4; Tissue-resident natural killer cell; Transglutaminase 2; Tubulointerstitial fibrosis
원문 및 링크아웃 정보
 
등재저널 정보