Lipoprotein lipase deficiency leads to α-synuclein aggregation and ubiquitin C-terminal hydrolase L1 reduction

H. Yang, T. Zhou, H. Wang, T. Liu, K. Ueda, R. Zhan, L. Zhao, Y. Tong, X. Tian, T. Zhang, Y. Jin, X. Han, Z. Li, Y. Zhao, X. Guo, W. Xiao, D. Fan, G. Liu, D. Chui

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

We have previously reported that presynaptic dysfunction and cognitive decline have been found in lipoprotein lipase (LPL) deficient mice, but the mechanism remains to be elucidated. Accumulating evidence supported that α-synuclein (α-syn) and ubiquitin C-terminal hydrolase L1 (UCHL1) are required for normal synaptic and cognitive function. In this study, we found that α-syn aggregated and the expression of UCHL1 decreased in the brain of LPL deficient mice. Reduction of UCHL1 was resulted from nuclear retention of DNA cytosine-5-methyltransferase 1 in LPL knockout mice. Reverse changes were found in cultured cells overexpressing LPL. Furthermore, deficiency of LPL increased ubiquitination of α-syn. These results indicated that aggregation of α-syn and reduction of UCHL1 expression in LPL-deficient mice may affect synaptic function.

Original languageEnglish (US)
Pages (from-to)1-10
Number of pages10
JournalNeuroscience
Volume290
DOIs
StatePublished - Apr 2 2015
Externally publishedYes

Keywords

  • DNA cytosine-5-methyltransferase 1
  • Lipoprotein lipase
  • Ubiquitin C-terminal hydrolase L1
  • α-synuclein

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint

Dive into the research topics of 'Lipoprotein lipase deficiency leads to α-synuclein aggregation and ubiquitin C-terminal hydrolase L1 reduction'. Together they form a unique fingerprint.

Cite this