■目前,没有证据表明细胞凋亡(CASP3)的表达,自噬(BECN1),和线粒体自噬(BNIP3)基因在CA3区缺血后长期存活。
■本文的目的是研究缺血6-24个月后CA3区上述基因表达的变化。
■在这项研究中,使用定量RT-PCR,我们介绍了在阿尔茨海默病的大鼠缺血模型中与神经元死亡相关的基因的表达。
■第一次,我们证实了CASP3基因在缺血后CA3区的过度表达,存活时间为0.5~2年.CASP3基因的过表达伴随着BECN1和BNIP3基因的活性水平在0.5年的时间内降低。然后,在1-2年内,BNIP3基因表达显着增加,并且与CASP3基因表达的增加相吻合。然而,BECN1基因表达是可变的,在缺血后1年和2年显着增加,低于对照值1.5年。
■我们的观察表明,长期存活的缺血通过与促凋亡基因BNIP3合作激活caspase3诱导CA3中的神经元死亡。该研究还表明BNIP3基因调节缺血后不依赖caspase的锥体细胞神经元死亡。因此,caspase依赖性和非依赖性神经元细胞的死亡发生在CA3区域缺血后。我们的数据表明BNIP3基因在调节CA3缺血后神经元死亡中的新作用。这表明BNIP3与CASP3一起参与缺血后神经元死亡。
UNASSIGNED: Currently, no evidence exists on the expression of apoptosis (CASP3), autophagy (BECN1), and mitophagy (BNIP3) genes in the CA3 area after ischemia with long-term survival.
UNASSIGNED: The goal of the paper was to study changes in above genes expression in CA3 area after ischemia in the period of 6-24 months.
UNASSIGNED: In this study, using quantitative RT-PCR, we present the expression of genes associated with neuronal death in a rat ischemic model of Alzheimer\'s disease.
UNASSIGNED: First time, we demonstrated overexpression of the CASP3 gene in CA3 area after ischemia with survival ranging from 0.5 to 2 years. Overexpression of the CASP3 gene was accompanied by a decrease in the activity level of the BECN1 and BNIP3 genes over a period of 0.5 year. Then, during 1-2 years, BNIP3 gene expression increased significantly and coincided with an increase in CASP3 gene expression. However, BECN1 gene expression was variable, increased significantly at 1 and 2 years and was below control values 1.5 years post-ischemia.
UNASSIGNED: Our observations suggest that ischemia with long-term survival induces neuronal death in CA3 through activation of caspase 3 in cooperation with the pro-apoptotic gene BNIP3. This study also suggests that the BNIP3 gene regulates caspase-independent pyramidal neuronal death post-ischemia. Thus, caspase-dependent and -independent death of neuronal cells occur post-ischemia in the CA3 area. Our data suggest new role of the BNIP3 gene in the regulation of post-ischemic neuronal death in CA3. This suggests the involvement of the BNIP3 together with the CASP3 in the CA3 in neuronal death post-ischemia.