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2018 ; 18
(1
): 322-332
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??synuclein induces apoptosis of astrocytes by causing dysfunction of the
endoplasmic reticulum?Golgi compartment
#MMPMID29749529
Liu M
; Qin L
; Wang L
; Tan J
; Zhang H
; Tang J
; Shen X
; Tan L
; Wang C
Mol Med Rep
2018[Jul]; 18
(1
): 322-332
PMID29749529
show ga
Although previous work has demonstrated that the overexpression of wild?type or
mutant ??synuclein (??syn) can induce cell death via a number of different
mechanisms, including oxidative stress, dysfunction of the ubiquitin?proteasome
degradation system, mitochondrial damage and endoplasmic reticulum (ER) stress,
research interest has primarily focused on neurons. However, there is
accumulating evidence that suggests that astrocytes may be involved in the
earliest changes, as well as the progression of Parkinson's disease (PD), though
the role of ??syn in astrocytes has not been widely studied. In the present
study, it was revealed that the mutant ??syn (A53T and A30P) in astrocytes
triggered ER stress via the protein kinase RNA?like ER kinase/eukaryotic
translation initiation factor 2? signaling pathway. Astrocyte apoptosis was
induced through a CCAAT?enhancer?binding protein homologous protein?mediated
pathway. In addition, Golgi fragmentation was observed in the process. On the
other hand, it was also demonstrated, in a primary neuronal?astroglial co?culture
system, that the overexpression of ??syn significantly decreased the levels of
glia?derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth.
Although direct evidence is currently lacking, it was proposed that dysfunction
of the ER?Golgi compartment in astrocytes overexpressing ??syn may lead to a
decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken
together, the results of the present study offer further insights into the
pathogenesis of PD from the perspective of astrocytes, which may provide novel
strategies for the diagnosis and treatment of PD in the future.
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