학술논문
miR-16-1 Promotes the aberrant [alpha]-synuclein accumulation in parkinson disease via targeting heat shock protein 70
Research Article
Research Article
Document Type
Report
Author
Source
The Scientific World Journal. Annual 2014, Vol. 14
Subject
Language
English
ISSN
1537-744X
Abstract
1. Introduction Parkinson disease (PD) is the second most common neurodegenerative disorder after Alzheimer disease [1], prominent characteristics of which include the degeneration of dopaminergic cells within the substantia nigra [...]
There is striking evidence that heat shock protein 70 (Hsp70) negatively regulates [alpha]-synuclein aggregation, which plays a significant role in the formation and progression of Parkinson disease (PD). However, how the Hsp70 in neurons fails to prevent or even reverse [alpha]-synuclein aggregation and toxicity in PD still remains to be determined. In the present study, we constructed an [alpha]-synuclein-overexpressed human neuroblastoma cell line, SH-SY5Y-Syn, in which the blockage of Hsp70 promoted [alpha]-synuclein aggregation. And we also found that miR-16-1 downregulated Hsp70 and promoted [alpha]-synuclein aggregation in the SH-SY5Y-Syn cells. This study revealed a novel regulatory mechanism of Hsp70 expression, which might contribute to the PD development.
There is striking evidence that heat shock protein 70 (Hsp70) negatively regulates [alpha]-synuclein aggregation, which plays a significant role in the formation and progression of Parkinson disease (PD). However, how the Hsp70 in neurons fails to prevent or even reverse [alpha]-synuclein aggregation and toxicity in PD still remains to be determined. In the present study, we constructed an [alpha]-synuclein-overexpressed human neuroblastoma cell line, SH-SY5Y-Syn, in which the blockage of Hsp70 promoted [alpha]-synuclein aggregation. And we also found that miR-16-1 downregulated Hsp70 and promoted [alpha]-synuclein aggregation in the SH-SY5Y-Syn cells. This study revealed a novel regulatory mechanism of Hsp70 expression, which might contribute to the PD development.