Class I HDAC s specifically regulate E‐cadherin expression in human renal epithelial cells
| العنوان: | Class I |
|---|---|
| المؤلفون: | Hae J. Kee, Ming Q. Lin, Thomas Kurz, Sin Y. Choi, Finn K. Hansen, Zhe Hao Piao, Yuhee Ryu, Myung Ho Jeong, Gwi Ran Kim, Li Jin |
| المصدر: | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE(20): 12 Journal of Cellular and Molecular Medicine |
| بيانات النشر: | Wiley, 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | 0301 basic medicine, Small interfering RNA, Epithelial-Mesenchymal Transition, Indoles, Pyridines, Down-Regulation, Biology, HK‐2 cells, Hydroxamic Acids, Histone Deacetylases, Cell Line, Kidney Tubules, Proximal, Transforming Growth Factor beta1, Extracellular matrix, 03 medical and health sciences, 0302 clinical medicine, epithelial‐mesenchymal transition (EMT), Antigens, CD, medicine, Humans, Extracellular Matrix Proteins, E‐cadherin, Cadherin, class I HDAC, epithelial-mesenchymal transition (EMT), renal fibrosis, HK-2 cells, E-cadherin, Epithelial Cells, HDAC8, Original Articles, Cell Biology, Transfection, Cadherins, HDAC4, Molecular biology, Cell biology, Histone Deacetylase Inhibitors, 030104 developmental biology, Trichostatin A, Gene Knockdown Techniques, 030220 oncology & carcinogenesis, Benzamides, Molecular Medicine, Original Article, Histone deacetylase, Biomarkers, medicine.drug |
| الوصف: | Epithelial-mesenchymal transition (EMT) and renal fibrosis are closely involved in chronic kidney disease. Inhibition of histone deacetylase (HDAC) has an anti-fibrotic effect in various diseases. However, the pathophysiological role of isoform-specific HDACs or class-selective HDACs in renal fibrosis remains unknown. Here, we investigated EMT markers and extracellular matrix (ECM) proteins in a human proximal tubular cell line (HK-2) by using HDAC inhibitors or by knockdown of class I HDACs (HDAC1, 2, 3 and 8). Trichostatin A (TSA), MS275, PCI34051 and LMK235 inhibited ECM proteins such as collagen type I or fibronectin in transforming growth factor beta 1 (TGF-beta 1)-induced HK2 cells. However, restoration of TGF-beta 1-induced E-cadherin down-regulation was only seen in HK-2 cells treated with TSA or MS275, but not with PCI34051, whereas TGF-beta 1-induced N-cadherin expression was not affected by the inhibitors. ECM protein and EMT marker levels were prevented or restored by small interfering RNA transfection against HDAC8, but not against other class I HDACs (HDAC1, 2 and 3). E-cadherin regulation is mediated by HDAC8 expression, but not by HDAC8 enzyme activity. Thus, class I HDACs (HDAC1, 2, 3 and 8) play a major role in regulating ECM and EMT, whereas class IIa HDACs (HDAC4 and 5) are less effective. |
| تدمد: | 1582-4934 1582-1838 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::56ae4f5916b3e4c46b50b87d315bcc35Test https://doi.org/10.1111/jcmm.12919Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....56ae4f5916b3e4c46b50b87d315bcc35 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15824934 15821838 |
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