Effect of HDAC-6 on PD cell induced by lactacystin

Li-Fei Xing; Dong-Tao Wang; Yu Yang; Su-Yue Pan

doi:10.1016/j.apjtm.2015.09.013

Effect of HDAC-6 on PD cell induced by lactacystin

Asian Pac J Trop Med. 2015 Oct;8(10):855-9. doi: 10.1016/j.apjtm.2015.09.013. Epub 2015 Sep 25.

Authors

Li-Fei Xing¹, Dong-Tao Wang², Yu Yang³, Su-Yue Pan⁴

Affiliations

¹ Nanfang Hospital, Southern Medical University, China; Department of Neurology, Inner Mongolia North Heavy Industries Group Corp. Ltd Hospital (The Third Affiliated Hospital of Baotou Medical College), China.
² Department of Thoracic Surgery, The Central Hospital, Baotou, Inner Mongolia, China.
³ Department of Endocrinology, Inner Mongolia North Heavy Industries Group Corp. Ltd Hospital (The Third Affiliated Hospital of Baotou Medical College), China.
⁴ Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: Pansuyue82@qq.com.

PMID: 26522302
DOI: 10.1016/j.apjtm.2015.09.013

Abstract

Objective: To explore the effects of histone deacetylase 6(HDAC-6) on the PD cell model induced by proteasome inhibitor lactacystin.

Methods: Human neuroblastoma SK-N-SH cells were cultured. The wild type pcDNA3.1-alpha-synuclein eukaryotic expression plasmid was transferred into the cells which then were divided into control group, group L, group T and group T+L. The cells of group L were added with 5 μmol/L lactacystin dissolved indimethylsulfoxide (DMSO) to induce PD cell model with abnormal protein aggregation, the cells of control group were treated with 5 μmol/L DMSO, the cells of group T were treated with 5 μmol/L selective HDAC-6 inhibitor tubacin dissolved in DMSO, and the cells of group T+L were treated with 5 μmol/L lactacystin and 10 μmol/L tubacin dissolved in DMSO. The expression levels of alpha-synuclein oligomers, HSP-27 and HSP-70 were detected by Western blot and the cell survival rate of all the groups was detected by MTT colorimetric assay, and compared 24 h after the cells were treated.

Results: The expression levels of alpha-synuclein oligomers, HSP-27 and HSP-70 of the cells of group L were significantly higher than the control group, and the cell survival rate was significantly lower (P < 0.05); the expression level of alpha-synuclein oligomers of the cells of group T+L was significantly higher than group L, but the expression level of HSP-27 and HSP-70 were significantly lower, and so as the cell survival rate (P < 0.05); the differences of the expression level of alpha-synuclein oligomers, HSP-27 and HSP-70 and the cell survival rate of the cells of group T and the control group were not statistically significant (P > 0.05).

Conclusions: The expression level of alpha-synuclein oligomers can be improved and the cell survival rate can be reduced by the PD cell model induced by lactacystin and treated with selective HDAC-6 inhibitor tubacin, which means that alpha-synuclein oligomers of the PD cell model induced by lactacystin can be inhibited and the cell survival rate can be improved by HDAC-6, and the mechanism may be related to the increased of HSP-27 and HSP-70.

Keywords: HDAC-6; Lactacystin; PD cell model.