期刊
AMERICAN JOURNAL OF ALZHEIMERS DISEASE AND OTHER DEMENTIAS
卷 35, 期 -, 页码 -出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1533317519883496
关键词
Alzheimer's disease; beta-hydroxybutyrate; tyrosine kinase receptor A; histonedeacetylases
资金
- Liaoning Provincial Natural Science Foundation of China [L20170541014]
Tyrosine kinase receptor A (TrkA) plays an important role in the protection of cholinergic neurons in Alzheimer's disease (AD). This study was designed to investigate whether beta-hydroxybutyrate (BHB), an endogenous histone deacetylase (HDAC) inhibitor, upregulates the expression of TrkA by affecting histone acetylation in SH-SY5Y cells treated with amyloid beta-protein (A beta). The results showed that BHB ameliorated the reduction of cell vitality and downregulation of TrkA expression induced by A beta. Furthermore, BHB inhibited the upregulation of HDAC1/2/3 expression and downregulation of histone acetylation (Ace-H3K9 and Ace-H4K12) levels in A beta-treated cells. The expression of TrkA was upregulated in HDAC1- or 3-silenced SH-SY5Y cells. However, there was no significant difference in TrkA expression between the HDAC2 knockdown and control cells. In conclusion, this study demonstrates that BHB protects against A beta-induced neurotoxicity in SH-SY5Y cells. The underlying mechanism of the effect may be associated with the upregulation of TrkA expression by inhibiting HDAC1/3.
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