Elevation of GM2 ganglioside during ethanol-induced apoptotic neurodegeneration in the developing mouse brain.
Elevation of GM2 ganglioside during ethanol-induced apoptotic neurodegeneration in the developing mouse brain.
复制标题
小鼠大脑发育过程中乙醇诱导的细胞凋亡性神经变性过程中 GM2 神经节苷脂的升高。
DOI：
10.1111/j.1471-4159.2012.07710.x
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发表时间：
2012
影响因子：
4.7
通讯作者：
Saito,Mariko
中科院分区：
文献类型：
--
作者：
Saito,Mitsuo;Chakraborty,Goutam;Shah,Relish;Mao,Rui-Fen;Kumar,Asok;Yang,Dun-Sheng;Dobrenis,Kostantin;Saito,Mariko
J. Neurochem.(2012)121, 649–661.AbstractGM2 ganglioside in the brain increased during ethanol‐induced acute apoptotic neurodegeneration in 7‐day‐old mice. A small but a significant increase observed 2 h after ethanol exposure was followed by a marked increase around 24 h. Subcellular fractionation of the brain 24 h after ethanol treatment indicated that GM2 increased in synaptic and non‐synaptic mitochondrial fractions as well as in a lysosome‐enriched fraction characteristic to the ethanol‐exposed brain. Immunohistochemical staining of GM2 in the ethanol‐treated brain showed strong punctate staining mainly in activated microglia, in which it partially overlapped with staining for LAMP1, a late endosomal/lysosomal marker. Also, there was weaker neuronal staining, which partially co‐localized with complex IV, a mitochondrial marker, and was augmented in cleaved caspase 3‐positive neurons. In contrast, the control brain showed only faint and diffuse GM2 staining in neurons. Incubation of isolated brain mitochondria with GM2in vitroinduced cytochromecrelease in a manner similar to that of GD3 ganglioside. Because ethanol is known to trigger mitochondria‐mediated apoptosis with cytochromecrelease and caspase 3 activation in the 7‐day‐old mouse brain, the GM2 elevation in mitochondria may be relevant to neuroapoptosis. Subsequently, activated microglia accumulated GM2, indicating a close relationship between GM2 and ethanol‐induced neurodegeneration.
