Increased numbers of oligodendrocyte lineage cells in the optic nerves of cerebroside sulfotransferase knockout mice
Increased numbers of oligodendrocyte lineage cells in the optic nerves of cerebroside sulfotransferase knockout mice
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DOI：
10.2183/pjab.87.415
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发表时间：
2011-07-01
影响因子：
3.1
通讯作者：
Baba, Hiroko
中科院分区：
文献类型：
--
作者：
Kajigaya, Hitoshi;Tanaka, Kenji F.;Baba, Hiroko
硫脂是一种髓磷脂糖脂，在体内参与节点旁轴-神经胶质连接的形成和体外调节少突胶质细胞分化。脑苷脂磺基转移酶 (CST) 催化少突胶质细胞谱系细胞中两种硫酸化糖脂、脑硫脂和前少突胶质细胞抗原的产生。最近的研究表明，在 CST 缺陷的条件下，从髓鞘形成阶段到成年期，大脑和脊髓中的少突胶质细胞显着增加。然而，这些是否是由于发育过程中的过度迁移或原位扩散造成的，尚不清楚。在本研究中，使用 CST 缺陷的视神经来检查硫酸糖脂缺陷条件下少突胶质细胞前体细胞 (OPC) 的迁移和增殖。 In adults, more NG2-positive OPCs and fully differentiated cells were observed.在视神经发育过程中，CST 缺陷小鼠和野生型小鼠中迁移前缘的细胞数量相似。然而，CST 缺陷小鼠中 BrdU(+) 增殖的 OPC 更为丰富。这些结果表明硫酸化糖脂可能参与OPCs体内增殖。
Sulfatide is a myelin glycolipid that functions in the formation of paranodal axo-glial junctions in vivo and in the regulation of oligodendrocyte differentiation in vitro. Cerebroside sulfotransferase (CST) catalyzes the production of two sulfated glycolipids, sulfatide and proligodendroblast antigen, in oligodendrocyte lineage cells. Recent studies have demonstrated significant increases in oligodendrocytes from the myelination stage through adulthood in brain and spinal cord under CST-deficient conditions. However, whether these result from excess migration or in situ proliferation during development is undetermined. In the present study, CST-deficient optic nerves were used to examine migration and proliferation of oligodendrocyte precursor cells (OPCs) under sulfated glycolipid-deficient conditions. In adults, more NG2-positive OPCs and fully differentiated cells were observed. In developing optic nerves, the number of cells at the leading edge of migration was similar in CST-deficient and wild-type mice. However, BrdU(+) proliferating OPCs were more abundant in CST-deficient mice. These results suggest that sulfated glycolipids may be involved in proliferation of OPCs in vivo.