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Transforming growth factor-beta 1 regulates human renal proximal tubular epithelial cell susceptibility to natural killer cells via modulation of the NKG2D ligands

Authors
Song, HyunkeunKim, YeonyePark, GabinKim, Yeong-SeokKim, SeonghanLee, Hyun-KyungChung, Woo YeongPark, Seok JuHan, Sang-YoubCho, DaehoHur, Daeyoung
Issue Date
Oct-2015
Publisher
SPANDIDOS PUBL LTD
Keywords
tubular epithelial cells; transforming growth factor-beta; natural killer cell; ischemia-reperfusion injury; NK group 2 member D
Citation
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.36, no.4, pp 1180 - 1188
Pages
9
Journal Title
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume
36
Number
4
Start Page
1180
End Page
1188
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10215
DOI
10.3892/ijmm.2015.2317
ISSN
1107-3756
1791-244X
Abstract
Transforming growth factor-beta (TGF-beta) has a significant role in the response to injury and tissue repair, and it has been detected in various cell types. However, the mechanism by which it regulates the response to ischemia-reperfusion injury (IRI) and manipulates natural killer (NK) cells is not well understood. In the present study, TGF-beta modulated NK cell function, thereby promoting recovery from renal IRI. Human renal proximal tubular epithelial cells (HK-2) treated with TGF-beta exhibited increased surface and intracellular expression of the NK group 2 member D (NKG2D) ligand MICA. This increased surface expression of MICA inhibited NK cell cytotoxicity to the HK-2 cells. In addition, an enzyme-linked immunosorbent assay revealed that TGF-beta treatment evidently increased the amount of soluble MICA released into the culture supernatant from HK-2 cells. Taken together, these findings suggest that TGF-beta-induced release of soluble MICA leads to downregulation of NKG2D, thereby preventing NK cell-mediated cytotoxicity toward renal proximal tubular epithelial cells in renal IRI, which in turn improves the survival of these cells.
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