Saitoh Yurika, Kamijo Akio, Yamauchi Junji, Sakamoto Takeharu, Terada Nobuo
Health Science Division, Department of Medical Sciences, Graduate School of Medicine, Science and Technology, Shinshu University, 3-1-1 Asahi, Matsumoto City, Nagano, 390-8621, Japan.
Center for Medical Education, Teikyo University of Science, Adachi-ku, Tokyo, Japan.
Histochem Cell Biol. 2019 May;151(5):385-394. doi: 10.1007/s00418-018-1745-y. Epub 2018 Oct 24.
A membrane skeletal molecular complex, protein 4.1G-membrane palmitoylated protein 6 (MPP6)-Lin7-cell adhesion molecule 4 (CADM4), is incorporated in Schwann cells, especially in Schmidt-Lanterman incisures (SLIs), in the mouse peripheral nervous system (PNS). MPP6, Lin7, and CADM4 are transported to SLIs by 4.1G. In this study, we created MPP6-deficient mice and evaluated myelin structure and MPP6 protein complexes. In SLIs in MPP6-deficient nerves, Lin7 was rarely detected by immunohistochemistry and western blotting, but the localization and amount of CADM4 and 4.1G were not altered. Motor activity was not significantly impaired in a tail-suspension test, but the sciatic nerves of MPP6-deficient mice had thicker myelin in internodes by electron microscopy compared to that of wild-type mice. These results indicate that the MPP6-Lin7 complex regulates myelin formation.
一种膜骨架分子复合物,即蛋白4.1G-膜棕榈酰化蛋白6(MPP6)-Lin7-细胞粘附分子4(CADM4),存在于小鼠外周神经系统(PNS)的雪旺细胞中,尤其是在施密特-兰特尔曼切迹(SLIs)中。MPP6、Lin7和CADM4通过4.1G转运至SLIs。在本研究中,我们创建了MPP6缺陷小鼠,并评估了髓鞘结构和MPP6蛋白复合物。在MPP6缺陷神经的SLIs中,免疫组织化学和蛋白质印迹法很少检测到Lin7,但CADM4和4.1G的定位和数量没有改变。在尾部悬吊试验中,运动活动没有受到显著损害,但与野生型小鼠相比,MPP6缺陷小鼠的坐骨神经节段的髓鞘在电镜下更厚。这些结果表明,MPP6-Lin7复合物调节髓鞘形成。