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2017 ; 40
(4
): 1125-1133
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English Wikipedia
Nova1 mediates resistance of rat pheochromocytoma cells to hypoxia-induced
apoptosis via the Bax/Bcl-2/caspase-3 pathway
#MMPMID28791345
Li H
; Lv B
; Kong L
; Xia J
; Zhu M
; Hu L
; Zhen D
; Wu Y
; Jia X
; Zhu S
; Cui H
Int J Mol Med
2017[Oct]; 40
(4
): 1125-1133
PMID28791345
show ga
Neuro-oncological ventral antigen 1 (Nova1) is a well known brain-specific
splicing factor. Several studies have identified Nova1 as a regulatory protein at
the top of a hierarchical network. However, the function of Nova1 during hypoxia
remains poorly understood. This study aimed to investigate the protective effect
of Nova1 against cell hypoxia and to further explore the Bax/Bcl-2/caspase-3
pathway as a potential mechanism. During hypoxia, the survival rate of
pheochromocytoma PC12 cells was gradually decreased and the apoptosis rate was
gradually increased, peaking at 48 h of hypoxia. At 48 h after transfection of
PC12 cells with pCMV-Myc-Nova1, the expression of Nova1 was significantly
increased, with wide distribution in the cytoplasm and nucleus. Moreover, the
survival rate was significantly increased and the apoptosis rate was
significantly decreased. Additionally, the mRNA and protein expression levels of
Bax and caspase-3 were significantly increased in the pCMV-Myc group and
significantly decreased in the pCMV?Myc-Nova1 group, whereas that of Bcl-2 was
significantly decreased in the pCMV-Myc group and significantly increased in the
pCMV-Myc-Nova1 group. This study indicated that Nova1 could be linked to
resistance to the hypoxia-induced apoptosis of PC12 cells via the
Bax/Bcl-2/caspase-3 pathway, and this finding may be of significance for
exploring novel mechanisms of hypoxia and the treatment of hypoxia-associated
diseases.