Roles of layilin in TNF-α-induced epithelial-mesenchymal transformation of renal tubular epithelial cells

Tumor necrosis factor (TNF)-α is suggested to induce epithelial-mesenchymal transformation (EMT) of renal tubular epithelial cells that possibly exacerbates renal interstitial fibrosis in glomerulonephritis (GN). We here investigated whether layilin (LAYN), a c-type lectin-homologous protein, was in...

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Published in:Biochemical and biophysical research communications 2015-11, Vol.467 (1), p.63-69
Main Authors: Adachi, Takayuki, Arito, Mitsumi, Suematsu, Naoya, Kamijo-Ikemori, Atsuko, Omoteyama, Kazuki, Sato, Toshiyuki, Kurokawa, Manae S., Okamoto, Kazuki, Kimura, Kenjiro, Shibagaki, Yugo, Kato, Tomohiro
Format: Article
Language:English
Subjects:
Adult
Animals
Carrier Proteins - metabolism
Cell Line
Epithelial Cells - cytology
Epithelial Cells - drug effects
Epithelial Cells - metabolism
Epithelial-mesenchymal transformation
Epithelial-Mesenchymal Transition - drug effects
Epithelial-Mesenchymal Transition - physiology
Female
Gene Knockdown Techniques
Glomerulonephritis
Glomerulonephritis - metabolism
Humans
Kidney Tubules - cytology
Kidney Tubules - drug effects
Kidney Tubules - metabolism
Layilin
Lectins, C-Type - antagonists & inhibitors
Lectins, C-Type - genetics
Lectins, C-Type - metabolism
Male
Membrane Glycoproteins - metabolism
Mice
Mice, Inbred ICR
Renal tubular epithelium
TNF-α
Tumor Necrosis Factor-alpha - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Young Adult
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Summary:Tumor necrosis factor (TNF)-α is suggested to induce epithelial-mesenchymal transformation (EMT) of renal tubular epithelial cells that possibly exacerbates renal interstitial fibrosis in glomerulonephritis (GN). We here investigated whether layilin (LAYN), a c-type lectin-homologous protein, was involved in the EMT process. Expression of LAYN was investigated in kidneys of mice administered with TNF-α and in a clear cell renal carcinoma cell line of KMRC-1 stimulated with TNF-α by quantitative polymerase chain reaction (qPCR) and/or western blotting. Expression of LAYN was assessed immunohistochemically in renal biopsy samples of patients with various types of GN. Changes of EMT markers and cell morphology by TNF-α and transforming growth factor (TGF)-β in LAYN-knocked down KMRC-1 cells were investigated by qPCR and immunocytochemistry. Administration of TNF-α increased expression of LAYN in renal tubular epithelia in mice. TNF-α but not TGF-β increased expression of LAYN in KMRC-1 cells. Renal biopsy samples from the patients with GN showed high expression of LAYN in tubular epithelial cells. TNF-α induced up-regulation of vimentin, down-regulation of E-cadherin, and fibroblast-like morphological change in KMRC-1 cells, indicating occurrence of EMT. These changes were not observed in the LAYN-knocked down cells. In contrast, similarly occurred TGF-β-induced EMT was not affected by the LAYN knockdown. Our data indicate that LAYN is involved in the TNF-α-induced EMT of renal tubular epithelial cells. LAYN may play roles in the generation of renal interstitial fibrosis in GN via TNF-α-induced EMT. •TNF-α enhances renal tubular expression of layilin in mice.•TNF-α enhances expression of layilin in a clear cell renal carcinoma cell line.•Patients with glomerulonephritis highly express layilin in their renal tubules.•Layilin is essential to induce epithelial-mesenchymal transformation by TNF-α.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2015.09.121