Objective: To assess whether histone deacetylase 4 (HDAC4) is related to the abnormal expression of α-synuclein (α-syn) via the autophagy pathway.

Background: The overexpression and aggregation of α-syn play central roles in the pathogenesis of Parkinson’s Disease (PD). Therefore, the clearance of α-syn is a feasible and promising therapeutics alternative for PD. Previous studies indicated that aberrant histone acetylation could inhibit the autophagy process, which influence the abnormal overexpression and aggregation of α-syn.

Methods: The shRNA of HDAC4 and vehicle were transfected into SH-SY5Y cells respectively, then the cells were treated with 1μmol rotenone for 48 hours. The protein levels of HDAC4, α-syn, LC3-Ⅱ, p62 and beclin-1 were evaluated by Western blot.

Results:  After exposure in rotenone, the SH-SY5Y cells showed an abnormal increase in the expression of α-syn. However, after knock-down of HDAC4, the abnormal expression of α-syn was reversed. Moreover, the protein levels of LC3-Ⅱ and belcin-1 were increased, while the level of p62 was decreased.

Conclusions: Reduced expression of HDAC4 reverses the abnormal expression of α-syn via activation of autophagy. HDAC4 is related to rotenone-induced elevated level of α-syn.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/genetic-knock-down-of-hdac4-attenuates-rotenone-induced-abnormal-expression-of-%ce%b1-synuclein-by-affecting-autophagic-flux-in-sh-sy5y-cells/