Abstract：
:Endoplasmic reticulum (ER) stress is linked to several neurological disorders, and neuronal injury cascades initiated by excessive ER stress are mediated, in part, via mitochondrial dysfunction. In the present study, we identified FAM3A as an important regulator of ER stress-induced cell death in neuronal HT22 cells. The ER stress inductor tunicamycin (TM) significantly decreased the expression of FAM3A at both mRNA and protein levels, which was shown to be dependent on the induction of reactive oxygen species (ROS). Overexpression of FAM3A attenuated TM-induced apoptosis and activation of ER stress factors, but had no effect on ER calcium metabolism in HT22 cells. We also found decreased mitochondrial ROS generation, inhibited cytochrome c release and preserved mitochondrial membrane potential (MMP) in FAM3A overexpressed cells. In addition, the experiments using isolated mitochondria showed that overexpression of FAM3A attenuated mitochondrial swelling and loss of mitochondrial Ca(2+) buffering capacity after TM exposure. By using specific targeted small interfering RNA (siRNA) to knockdown the expression of the C/EBP homologous protein (CHOP), we found that FAM3A-induced protection and inhibition of ER stress was mediated by inverting TM-induced decrease of Wnt through the CHOP pathway. Our study demonstrates a pivotal role of FAM3A in protecting against TM-induced cytotoxicity via regulating CHOP-Wnt pathway, and suggests the therapeutic values of FAM3A overexpression against ER stress-associated neuronal injury.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Song Q,Gou WL,Zhang Rdoi
10.1016/j.neuint.2016.02.010subject
Has Abstractpub_date
2016-03-01 00:00:00pages
82-9eissn
0197-0186issn
1872-9754pii
S0197-0186(16)30019-5journal_volume
94pub_type
杂志文章abstract：:Long-term potentiation (LTP) is a well-established experimental model used to investigate the synaptic basis of learning and memory. LTP at mossy fibre - CA3 synapses in the hippocampus is unusual because it is normally N-methyl-d-aspartate (NMDA) receptor-independent. Instead it seems that the trigger for mossy fibre...
journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
pub_type： 杂志文章,评审
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journal_title：Neurochemistry international
pub_type： 杂志文章
doi：10.1016/j.neuint.2007.01.007
更新日期：2007-04-01 00:00:00
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
pub_type： 传,历史文章,杂志文章
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
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