Korean Circulation Journal

The Korean Society of Cardiology (대한심장학회)
권호 표지
DOI QR코드

DOI QR Code

Expression of Class I and Class II a/b Histone Deacetylase is Dysregulated in Hypertensive Animal Models

  • Kee, Hae Jin (Heart Research Center of Chonnam National University Hospital) ;
  • Kim, Gwi Ran (Heart Research Center of Chonnam National University Hospital) ;
  • Lin, Ming Quan (Heart Research Center of Chonnam National University Hospital) ;
  • Choi, Sin Young (Heart Research Center of Chonnam National University Hospital) ;
  • Ryu, Yuhee (Heart Research Center of Chonnam National University Hospital) ;
  • Jin, Li (Heart Research Center of Chonnam National University Hospital) ;
  • Piao, Zhe Hao (The Second Hospital of Jilin University) ;
  • Jeong, Myung Ho (Heart Research Center of Chonnam National University Hospital)
  • Received : 2016.07.17
  • Accepted : 2016.10.07
  • Published : 2017.05.31
⟨ Previous Next ⟩

Abstract

Background and Objectives: Dysregulation of histone deacetylase expression and enzymatic activity is associated with a number of diseases. It has been reported that protein levels of histone deacetylase (HDAC)1 and HDAC5 increase during human pulmonary hypertension, and that the enzymatic activity of HDAC6 is induced in a chronic hypertensive animal model. This study investigated the protein expression profiles of class I and II a/b HDACs in three systemic hypertension models. Materials and Methods: We used three different hypertensive animal models: (i) Wistar-Kyoto rats (n=8) and spontaneously hypertensive rats (SHR; n=8), (ii) mice infused with saline or angiotensin II to induce hypertension, via osmotic mini-pump for 2 weeks, and (iii) mice that were allowed to drink L-$N^G$-nitro-L-arginine methyl ester (L-NAME) to induce hypertension. Results: SHR showed high systolic, diastolic, and mean blood pressures. Similar increases in systolic blood pressure were observed in angiotensin II or L-NAME-induced hypertensive mice. In SHR, class IIa HDAC (HDAC4, 5, and 7) and class IIb HDAC (HDAC6 and 10) protein expression were significantly increased. In addition, a HDAC3 protein expression was induced in SHR. However, in L-NAME mice, class IIa HDAC protein levels (HDAC4, 5, 7, and 9) were significantly reduced. HDAC8 protein levels were significantly reduced both in angiotensin II mice and in SHR. Conclusion: These results indicate that dysregulation of class I and class II HDAC protein is closely associated with chronic hypertension.

Keywords

Acknowledgement

Supported by : Korean Society of Cardiology

References

  1. Ribeiro MO, Antunes E, de Nucci G, Lovisolo SM, Zatz R. Chronic inhibition of nitric oxide synthesis. A new model of arterial hypertension. Hypertension 1992;20:298-303. https://doi.org/10.1161/01.HYP.20.3.298
  2. Brand S, Amann K, Schupp N. Angiotensin II-induced hypertension dose-dependently leads to oxidative stress and DNA damage in mouse kidneys and hearts. J Hypertens 2013;31:333-44. https://doi.org/10.1097/HJH.0b013e32835ba77e
  3. Ler SY, Leung CH, Khin LW, et al. HDAC1 and HDAC2 independently predict mortality in hepatocellular carcinoma by a competing risk regression model in a southeast Asian population. Oncol Rep 2015;34:2238-50. https://doi.org/10.3892/or.2015.4263
  4. Koumangoye RB, Andl T, Taubenslag KJ, et al. SOX4 interacts with EZH2 and HDAC3 to suppress microRNA-31 in invasive esophageal cancer cells. Mol Cancer 2015;14:24. https://doi.org/10.1186/s12943-014-0284-y
  5. Wilson AJ, Byun DS, Popova N, et al. Histone deacetylase 3 (HDAC3) and other class I HDACs regulate colon cell maturation and p21 expression and are deregulated in human colon cancer. J Biol Chem 2006;281:13548-58. https://doi.org/10.1074/jbc.M510023200
  6. Li S, Wang B, Xu Y, Zhang J. Autotaxin is induced by TSA through HDAC3 and HDAC7 inhibition and antagonizes the TSA-induced cell apoptosis. Mol Cancer 2011;10:18. https://doi.org/10.1186/1476-4598-10-18
  7. Lee HA, Lee DY, Cho HM, Kim SY, Iwasaki Y, Kim IK. Histone deacetylase inhibition attenuates transcriptional activity of mineralocorticoid receptor through its acetylation and prevents development of hypertension. Circ Res 2013;112:1004-12. https://doi.org/10.1161/CIRCRESAHA.113.301071
  8. Lee HA, Song MJ, Seok YM, Kang SH, Kim SY, Kim I. Histone deacetylase 3 and 4 complex stimulates the transcriptional activity of the mineralocorticoid receptor. PLoS One 2015;10:e0136801. https://doi.org/10.1371/journal.pone.0136801
  9. Usui T, Okada M, Mizuno W, et al. HDAC4 mediates development of hypertension via vascular inflammation in spontaneous hypertensive rats. Am J Physiol Heart Circ Physiol 2012;302:H1894-904. https://doi.org/10.1152/ajpheart.01039.2011
  10. Kameshima S, Okada M, Yamawaki H. Expression and localization of calmodulin-related proteins in brain, heart and kidney from spontaneously hypertensive rats. Biochem Biophys Res Commun 2016;469:654-8. https://doi.org/10.1016/j.bbrc.2015.12.048
  11. Cavasin MA, Demos-Davies K, Horn TR, et al. Selective class I histone deacetylase inhibition suppresses hypoxia-induced cardiopulmonary remodeling through an antiproliferative mechanism. Circ Res 2012;110:739-48. https://doi.org/10.1161/CIRCRESAHA.111.258426
  12. Pang J, Yan C, Natarajan K, et al. GIT1 mediates HDAC5 activation by angiotensin II in vascular smooth muscle cells. Arterioscler Thromb Vasc Biol 2008;28:892-8. https://doi.org/10.1161/ATVBAHA.107.161349
  13. Kee HJ, Bae EH, Park S, et al. HDAC inhibition suppresses cardiac hypertrophy and fibrosis in DOCA-salt hypertensive rats via regulation of HDAC6/HDAC8 enzyme activity. Kidney Blood Press Res 2013;37:229-39. https://doi.org/10.1159/000350148
  14. Lemon DD, Horn TR, Cavasin MA, et al. Cardiac HDAC6 catalytic activity is induced in response to chronic hypertension. J Mol Cell Cardiol 2011;51:41-50. https://doi.org/10.1016/j.yjmcc.2011.04.005
  15. 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. https://doi.org/10.1016/j.vph.2015.04.006
  16. Kee HJ, Kwon JS, Shin S, Ahn Y, Jeong MH, Kook H. Trichostatin A prevents neointimal hyperplasia via activation of Kruppel like factor 4. Vascul Pharmacol 2011;55:127-34. https://doi.org/10.1016/j.vph.2011.07.001
  17. Xu X, Ha CH, Wong C, et al. Angiotensin II stimulates protein kinase D-dependent histone deacetylase 5 phosphorylation and nuclear export leading to vascular smooth muscle cell hypertrophy. Arterioscler Thromb Vasc Biol 2007;27:2355-62. https://doi.org/10.1161/ATVBAHA.107.151704
  18. Usui T, Morita T, Okada M, Yamawaki H. Histone deacetylase 4 controls neointimal hyperplasia via stimulating proliferation and migration of vascular smooth muscle cells. Hypertension 2014;63:397-403. https://doi.org/10.1161/HYPERTENSIONAHA.113.01843
  19. Kim GR, Cho SN, Kim HS, et al. HDAC4 and GATA6 regulate arterial remodeling in angiotensin ii-induced hypertension. J Hypertens 2016;34:2206-19. https://doi.org/10.1097/HJH.0000000000001081
  20. Baylis C, Mitruka B, Deng A. Chronic blockade of nitric oxide synthesis in the rat produces systemic hypertension and glomerular damage. J Clin Invest 1992;90:278-81. https://doi.org/10.1172/JCI115849
  21. Bartunek J, Weinberg EO, Tajima M, et al. Chronic N(G)-nitro-L-arginine methyl ester-induced hypertension: novel molecular adaptation to systolic load in absence of hypertrophy. Circulation 2000;101:423-9. https://doi.org/10.1161/01.CIR.101.4.423
  22. Lucio-Eterovic AK, Cortez MA, Valera ET, et al. Differential expression of 12 histone deacetylase (HDAC) genes in astrocytomas and normal brain tissue: class II and IV are hypoexpressed in glioblastomas. BMC Cancer 2008;8:243. https://doi.org/10.1186/1471-2407-8-243

피인용 문헌

  1. Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension vol.14, pp.3, 2017, https://doi.org/10.1371/journal.pone.0213186
  2. Sodium butyrate attenuates angiotensin II‐induced cardiac hypertrophy by inhibiting COX2/PGE2 pathway via a HDAC5/HDAC6‐dependent mechanism vol.23, pp.12, 2019, https://doi.org/10.1111/jcmm.14684
  3. Dissecting Histone Deacetylase 3 in Multiple Disease Conditions: Selective Inhibition as a Promising Therapeutic Strategy vol.64, pp.13, 2017, https://doi.org/10.1021/acs.jmedchem.0c01676