Class I HDACs specifically regulate E-cadherin expression in human renal epithelial cells

Journal of Cellular and Molecular Medicine

Volumn 20, Issue 12, 2016, Pages 2289-2298

  Choi, Sin Y ^a   Kee, Hae J ^a   Kurz, Thomas ^b   Hansen, Finn K ^b   Ryu, Yuhee ^a   Kim, Gwi R ^a   Lin, Ming Q ^a   Jin, Li ^a,c   Piao, Zhe H ^a,d   Jeong, Myung H ^a  

^a Chonnam National University Medical School   (South Korea)

^b HEINRICH HEINE UNIVERSITY   (Germany)

^c Affiliated Jilin Hospital of Jilin University   (China)

^d THE SECOND HOSPITAL OF JILIN UNIVERSITY   (China)

Author keywords

class I HDAC; E cadherin; epithelial mesenchymal transition (EMT); HK 2 cells; renal fibrosis

Indexed keywords

ALPHA SMOOTH MUSCLE ACTIN; CADHERIN; COLLAGEN TYPE 1; HISTONE DEACETYLASE; HISTONE DEACETYLASE 1; HISTONE DEACETYLASE 2; HISTONE DEACETYLASE 3; HISTONE DEACETYLASE 4; HISTONE DEACETYLASE 5; HISTONE DEACETYLASE INHIBITOR; SMALL INTERFERING RNA; TRANSFORMING GROWTH FACTOR BETA1; TRICHOSTATIN A; UVOMORULIN; BENZAMIDE DERIVATIVE; BIOLOGICAL MARKER; CDH1 PROTEIN, HUMAN; ENTINOSTAT; HYDROXAMIC ACID; INDOLE DERIVATIVE; PCI 34051; PYRIDINE DERIVATIVE; SCLEROPROTEIN;

ARTICLE; CELL VIABILITY ASSAY; CYTOTOXICITY; DOWN REGULATION; ENZYME ACTIVITY; EPITHELIAL MESENCHYMAL TRANSITION; EXTRACELLULAR MATRIX; GENE EXPRESSION REGULATION; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; IMMUNOCYTOCHEMISTRY; IMMUNOFLUORESCENCE; KIDNEY EPITHELIUM; MTT ASSAY; PRIORITY JOURNAL; PROTEIN EXPRESSION; REAL TIME POLYMERASE CHAIN REACTION; WESTERN BLOTTING; CELL LINE; CYTOLOGY; DRUG EFFECTS; EPITHELIUM CELL; GENE SILENCING; KIDNEY PROXIMAL TUBULE; METABOLISM;

BENZAMIDES; BIOMARKERS; CADHERINS; CELL LINE; DOWN-REGULATION; EPITHELIAL CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; EXTRACELLULAR MATRIX PROTEINS; GENE KNOCKDOWN TECHNIQUES; HISTONE DEACETYLASE INHIBITORS; HISTONE DEACETYLASES; HUMANS; HYDROXAMIC ACIDS; INDOLES; KIDNEY TUBULES, PROXIMAL; PYRIDINES; TRANSFORMING GROWTH FACTOR BETA1;

EID: 84978374816     PISSN: 15821838     EISSN: None     Source Type: Journal    
DOI: 10.1111/jcmm.12919     Document Type: Article

References (29)

1. Nakatsuji S, Yamate J, Sakuma S. Macrophages, myofibroblasts, and extracellular matrix accumulation in interstitial fibrosis of chronic progressive nephropathy in aged rats. Vet Pathol. 1998; 35: 352–60.
2. Tonelli M, Wiebe N, Culleton B, et al. Chronic kidney disease and mortality risk: a systematic review. J Am Soc Nephrol. 2006; 17: 2034–47.
3. Vieira JM Jr, Mantovani E, Rodrigues LT, et al. Simvastatin attenuates renal inflammation, tubular transdifferentiation and interstitial fibrosis in rats with unilateral ureteral obstruction. Nephrol Dial Transplant. 2005; 20: 1582–91.
4. Pohlers D, Brenmoehl J, Loffler I, et al. TGF-beta and fibrosis in different organs – molecular pathway imprints. Biochim Biophys Acta. 2009; 1792: 746–56.
5. Kalluri R, Weinberg RA. The basics of epithelial-mesenchymal transition. J Clin Invest. 2009; 119: 1420–8.
6. Burns WC, Thomas MC. The molecular mediators of type 2 epithelial to mesenchymal transition (EMT) and their role in renal pathophysiology. Expert Rev Mol Med. 2010; 12: e17.
7. Rastaldi MP. Epithelial-mesenchymal transition and its implications for the development of renal tubulointerstitial fibrosis. J Nephrol. 2006; 19: 407–12.
8. Gottlicher M, Minucci S, Zhu P, et al. Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells. EMBO J. 2001; 20: 6969–78.
9. Adcock IM. HDAC inhibitors as anti-inflammatory agents. Br J Pharmacol. 2007; 150: 829–31.
10. Pang M, Kothapally J, Mao H, et al. Inhibition of histone deacetylase activity attenuates renal fibroblast activation and interstitial fibrosis in obstructive nephropathy. Am J Physiol Renal Physiol. 2009; 297: F996–1005.
11. Ji M, Lee EJ, Kim KB, et al. HDAC inhibitors induce epithelial-mesenchymal transition in colon carcinoma cells. Oncol Rep. 2015; 33: 2299–308.
12. Lei W, Zhang K, Pan X, et al. Histone deacetylase 1 is required for transforming growth factor-beta1-induced epithelial-mesenchymal transition. Int J Biochem Cell Biol. 2010; 42: 1489–97.
13. Noh H, Oh EY, Seo JY, et al. Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury. Am J Physiol Renal Physiol. 2009; 297: F729–39.
14. Shan B, Yao TP, Nguyen HT, et al. Requirement of HDAC6 for transforming growth factor-beta1-induced epithelial-mesenchymal transition. J Biol Chem. 2008; 283: 21065–73.
15. Marek L, Hamacher A, Hansen FK, et al. Histone deacetylase (HDAC) inhibitors with a novel connecting unit linker region reveal a selectivity profile for HDAC4 and HDAC5 with improved activity against chemoresistant cancer cells. J Med Chem. 2013; 56: 427–36.
16. Kee HJ, Kim JR, Nam KI, et al. Enhancer of polycomb1, a novel homeodomain only protein-binding partner, induces skeletal muscle differentiation. J Biol Chem. 2007; 282: 7700–9.
17. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001; 25: 402–8.
18. Leask A. TGFbeta, cardiac fibroblasts, and the fibrotic response. Cardiovasc Res. 2007; 74: 207–12.
19. Sousa AM, Liu T, Guevara O, et al. Smooth muscle alpha-actin expression and myofibroblast differentiation by TGFbeta are dependent upon MK2. J Cell Biochem. 2007; 100: 1581–92.
20. Kiesslich T, Pichler M, Neureiter D. Epigenetic control of epithelial-mesenchymal-transition in human cancer. Mol Clin Oncol. 2013; 1: 3–11.
21. Iwano M, Plieth D, Danoff TM, et al. Evidence that fibroblasts derive from epithelium during tissue fibrosis. J Clin Invest. 2002; 110: 341–50.
22. Hu E, Dul E, Sung CM, et al. Identification of novel isoform-selective inhibitors within class I histone deacetylases. J Pharmacol Exp Ther. 2003; 307: 720–8.
23. Liu N, He S, Ma L, et al. Blocking the class I histone deacetylase ameliorates renal fibrosis and inhibits renal fibroblast activation via modulating TGF-beta and EGFR signaling. PLoS ONE. 2013; 8: e54001.
24. Choi SY, Ryu Y, Kee HJ, et al. Tubastatin A suppresses renal fibrosis via regulation of epigenetic histone modification and Smad3-dependent fibrotic genes. Vascul Pharmacol. 2015; 72: 130–40.
25. Carew RM, Wang B, Kantharidis P. The role of EMT in renal fibrosis. Cell Tissue Res. 2012; 347: 103–16.
26. Yoshikawa M, Hishikawa K, Marumo T, et al. Inhibition of histone deacetylase activity suppresses epithelial-to-mesenchymal transition induced by TGF-beta1 in human renal epithelial cells. J Am Soc Nephrol. 2007; 18: 58–65.
27. Jurkin J, Zupkovitz G, Lagger S, et al. Distinct and redundant functions of histone deacetylases HDAC1 and HDAC2 in proliferation and tumorigenesis. Cell Cycle. 2011; 10: 406–12.
28. Ma P, Pan H, Montgomery RL, et al. Compensatory functions of histone deacetylase 1 (HDAC1) and HDAC2 regulate transcription and apoptosis during mouse oocyte development. Proc Natl Acad Sci USA. 2012; 109: E481–9.
29. Godman CA, Joshi R, Tierney BR, et al. HDAC3 impacts multiple oncogenic pathways in colon cancer cells with effects on Wnt and vitamin D signaling. Cancer Biol Ther. 2008; 7: 1570–80.