Deficiency of primary cilia in kidney epithelial cells induces epithelial to mesenchymal transition
| Autor: | Jin Ki Jung, Kwon Moo Park, Seong-Ryong Lee, Jee In Kim, Byeong-Churl Jang, Sang Jun Han, Seung Soon Im |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Epithelial-Mesenchymal Transition Biophysics Biochemistry Madin Darby Canine Kidney Cells 03 medical and health sciences 0302 clinical medicine Dogs Microtubule Transforming Growth Factor beta Tubulin Animals Epithelial–mesenchymal transition Cilia RNA Small Interfering Molecular Biology Actin Cell Size biology Chemistry ADP-Ribosylation Factors Cilium Mesenchymal stem cell Cell Biology Transforming growth factor beta Actins Cell biology Fibronectins Fibronectin 030104 developmental biology Collagen Type III Gene Expression Regulation 030220 oncology & carcinogenesis embryonic structures biology.protein Signal transduction Carrier Proteins Signal Transduction |
| Zdroj: | Biochemical and biophysical research communications. 496(2) |
| ISSN: | 1090-2104 |
| Popis: | Primary cilium is a microtubule-based non-motile organelle that plays critical roles in kidney pathophysiology. Our previous studies revealed that the lengths of primary cilia decreased upon renal ischemia/reperfusion injury and oxidative stress, and restored with recovery. Here, we tested the hypothesis that lack of primary cilium causes epithelial to mesenchymal transition (EMT) of kidney tubule cells. We investigated the alteration of length of primary cilia in TGF-β-induced EMT via visualization of primary cilia by fluorescence staining against acetylated α-tubulin. EMT was determined by measuring mesenchymal protein expression using quantitative PCR and indirect fluorescence staining. As a result, TGF-β treatment decreased ciliary length along with EMT. To test whether defect of primary cilia trigger onset of EMT, cilia formation was disturbed by knock down of ciliary protein using siRNA along with/without TGF-β treatment. Knock down of Arl13b and Ift20 reduced cilia elongation and increased expression of EMT markers such as fibronectin, α-SMA, and collagen III. TGF-β-induced EMT was greater as well in Arl13b and Ift20-knock down cells compared to control cells. Taken together, deficiency of primary cilia trigger EMT and exacerbates it under pro-fibrotic signals. |
| Databáze: | OpenAIRE |
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