Ohtsuka-Tsurumi Eiko, Saito Yoshiaki, Yamamoto Tomoko, Voit Thomas, Kobayashi Makio, Osawa Makiko
Department of Pediatrics, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
Brain Res Dev Brain Res. 2004 Sep 17;152(2):121-7. doi: 10.1016/j.devbrainres.2004.06.006.
Hypoglycosylation of alpha-dystroglycan (alpha-DG) has been identified in several human diseases associated with muscular dystrophy and brain malformations, including Fukuyama-type congenital muscular dystrophy (FCMD) caused by mutations in the fukutin gene. Although disruption of the intra-extra membrane linkage in the sarcolemma via the dystroglycan (DG) has been hypothesized as a possible underlying mechanism, little is known about the pathogenesis of brain anomalies in these conditions. In this study, we examined the patterns of expression of fukutin and alpha-DG in developing and adult mouse brains. Antisera against fukutin and alpha-DG identified neurons of the fetal cerebral and cerebellar cortex and the subpial pontine migratory stream. In adult mice, fukutin and alpha-DG were extensively co-expressed in neurons of the cerebral and cerebellar cortex, hippocampus, basal ganglia and olfactory bulb, as well as in the pontine nucleus and the cranial nerve nuclei. These results support the hypothesis that fukutin is involved in the glycosylation process of alpha-DG and that a defect in this process plays an essential role in the pathogenesis of FCMD. Further research into the physiological function of alpha-DG in migrating and mature neurons is required.
α-肌营养不良蛋白聚糖(α-DG)的低糖基化已在几种与肌肉萎缩症和脑畸形相关的人类疾病中被发现,包括由福库汀基因(fukutin)突变引起的福山型先天性肌营养不良(FCMD)。尽管通过肌营养不良蛋白聚糖(DG)破坏肌膜中的膜内-膜外连接被认为是一种可能的潜在机制,但对于这些情况下脑异常的发病机制知之甚少。在本研究中,我们检测了福库汀和α-DG在发育中和成年小鼠脑中的表达模式。抗福库汀和α-DG的抗血清鉴定出胎儿大脑和小脑皮质以及软膜下脑桥迁移流中的神经元。在成年小鼠中,福库汀和α-DG在大脑和小脑皮质、海马体、基底神经节和嗅球的神经元中广泛共表达,以及在脑桥核和脑神经核中也有表达。这些结果支持了以下假设:福库汀参与α-DG的糖基化过程,并且该过程中的缺陷在FCMD的发病机制中起重要作用。需要进一步研究α-DG在迁移和成熟神经元中的生理功能。