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, Hyunkeun; Kim, Yeonye; Park, Gabin; Kim, Yeong-Seok; Kim, Seonghan; Lee, Hyun-Kyung; Chung, Woo Yeong; Park, Seok Ju; Han, Sang-Youb; Cho, Daeho; Hur, 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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