دورية أكاديمية
Indoxyl sulfate-induced epithelial-to-mesenchymal transition and apoptosis of renal tubular cells as novel mechanisms of progression of renal disease.
| العنوان: | Indoxyl sulfate-induced epithelial-to-mesenchymal transition and apoptosis of renal tubular cells as novel mechanisms of progression of renal disease. |
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| المؤلفون: | Kim SH; Division of Nephrology, Department of Internal Medicine, Chung-Ang University, Seoul, Korea., Yu MA, Ryu ES, Jang YH, Kang DH |
| المصدر: | Laboratory investigation; a journal of technical methods and pathology [Lab Invest] 2012 Apr; Vol. 92 (4), pp. 488-98. Date of Electronic Publication: 2012 Jan 09. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Inc Country of Publication: United States NLM ID: 0376617 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1530-0307 (Electronic) Linking ISSN: 00236837 NLM ISO Abbreviation: Lab Invest Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2023- : [New York] : Elsevier Inc. Original Publication: Baltimore : Williams & Wilkins |
| مواضيع طبية MeSH: | Apoptosis* , Epithelial-Mesenchymal Transition*, Indican/*metabolism , Renal Insufficiency, Chronic/*metabolism, Actins/metabolism ; Animals ; Cadherins/metabolism ; Cell Line ; Cell Movement ; Cell Proliferation ; Disease Progression ; Enzyme Activation ; Membrane Proteins/metabolism ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 1/metabolism ; Phosphoproteins/metabolism ; Rats ; Signal Transduction ; Zonula Occludens-1 Protein ; p38 Mitogen-Activated Protein Kinases/metabolism |
| مستخلص: | Indoxyl sulfate (IS), one of the uremic toxins, is regarded to have a substantial role in the progression of chronic kidney disease (CKD). Epithelial-to-mesenchymal transition (EMT) and apoptosis of renal tubular cells are known to be the critical mechanisms of the development and aggravation of CKD. We investigated the effect of IS on EMT and apoptosis in renal proximal tubular cells, NRK-52E cells. IS significantly inhibited cell proliferation and induced cell migration with a morphological transition from cuboidal epithelial cells to spindle-shaped scattered fibroblast-like cells. IS downregulated the expressions of zonula occluden-1 and E-cadherin, whereas upregulated α-SMA expression at 48 h, which was blocked by a pretreatment of the organic anion transporter, probenecid. IS also induced apoptosis of NRK cells from a concentration of 25 μg/ml with an activation of ERK1/2 and p38 MAP kinase (MAPK). Pretreatment of ERK1/2 or p38 MAPK inhibitors, PD98059 or SB203580, resulted in no significant effect on IS-induced EMT, whereas it ameliorated IS-induced apoptosis of NRK cells. These findings suggested phenotypic transition and apoptosis as potential mechanisms of IS-induced renal damage and the differential role of MAPK activation in IS-induced EMT and apoptosis of renal tubular cells. |
| المشرفين على المادة: | 0 (Actins) 0 (Cadherins) 0 (Membrane Proteins) 0 (Phosphoproteins) 0 (Tjp1 protein, rat) 0 (Zonula Occludens-1 Protein) 0 (smooth muscle actin, rat) EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1) EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) N187WK1Y1J (Indican) |
| تواريخ الأحداث: | Date Created: 20120111 Date Completed: 20120522 Latest Revision: 20230216 |
| رمز التحديث: | 20230216 |
| DOI: | 10.1038/labinvest.2011.194 |
| PMID: | 22231736 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1530-0307 |
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| DOI: | 10.1038/labinvest.2011.194 |