Korean Circulation Journal

The Korean Society of Cardiology (대한심장학회)
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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
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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

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