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Tissue-resident natural killer cells exacerbate tubulointerstitial fibrosis by activating transglutaminase 2 and syndecan-4 in a model of aristolochic acid-induced nephropathy
Yu Mee Wee1, Heounjeong Go2, Monica Young Choi1, Hey Rim Jung1, Yong Mee Cho2, Young Hoon Kim3, Duck Jong Han3, Sung Shin1,3,*
1Asan Institute for life science, Asan Medical Center,
2Pathology and 3Surgery, Asan Medical Center and University of Ulsan college of Medicine
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 depletion of trNK cells may ameliorate renal fibrosis by affecting transglutaminase 2/syndecan-4 interactions. C57BL/6 mice treated with anti-asialo GM1 (ASGM1) or NK1.1 antibody were subjected to aristolochic acid nephropathy (AAN) as an experimental model of kidney fibrosis. Although both ASGM1 and NK1.1 antibody suppressed renal NKp46+DX5+ NK cells, renal NKp46+DX5− cells were resistant to suppression by ASGM1 or NK1.1 antibody during the development of tubulointerstitial fibrosis in the AAN model. Western blot analysis showed that both antibodies increased the expression of fibronectin, transglutaminase 2 and syndecan-4. These findings indicate that trNK cells play an excerbative role in tubulointerstitial fibrosis by activating transglutaminase 2 and syndecan-4 in the AAN model.
Abstract, Accepted Manuscript(in press) [Submitted on August 23, 2018, Accepted on December 26, 2018]
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