Leptin affects oligodendroglial development in the mouse embryonic cerebral cortex.

Leptin affects oligodendroglial development in the mouse embryonic cerebral cortex.
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发表时间:
2006-02
期刊:
Neuro endocrinology letters
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通讯作者:
J. Udagawa;M. Nimura;H. Otani
J. Udagawa;M. Nimura;H. Otani
中科院分区:
其他
文献类型:
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作者:
J. Udagawa;M. Nimura;H. Otani

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瘦素是一种肥胖基因产物,可降低成人食欲并增加能量消耗。在我们之前的研究中,瘦素被发现维持神经干细胞和/或祖细胞,优先是星形胶质细胞/少突胶质细胞祖细胞,而减少少突胶质细胞谱系限制性前体细胞的比例。据报道,瘦素缺乏(ob/ob)小鼠的神经胶质蛋白水平低于野生型小鼠。这些发现表明瘦素影响神经胶质细胞的发育。因此,在本研究中,我们通过组织化学方法研究了ob/ob和野生型小鼠胚胎大脑皮层少突胶质细胞的发育。方法在胚胎日(E) 18获得ob/ob或野生型(C57BL/6J)胚胎。我们在胚胎大脑中使用抗NG2、血小板衍生生长因子受体α (pdgfr - α)和瘦素受体(Ob-R)的抗体进行免疫组化。在大脑皮层,我们比较了ob/ob和野生型胚胎中NG2和/或pdgfr - α免疫阳性的少突胶质细胞前体细胞(OPCs)的数量。结果E18上ob/ob胚的OPCs明显高于野生型胚。pdgfr - α阳性的OPCs在大脑皮层中不共表达瘦素受体。结论瘦素抑制小鼠胚胎大脑皮层多能性和/或胶质祖细胞向OPCs的分化,但不直接作用于OPCs。
OBJECTIVE Leptin, which is an obese gene product, decreases appetite and increases energy expenditure in adults. In our previous study, leptin was found to maintain neural stem cells and/or progenitor cells, preferentially astrocyte/oligodendrocyte progenitor cells, whereas it reduces the proportion of oligodendrocyte lineage-restricted precursor cells. It has been reported that leptin-deficient (ob/ob) mice have lower levels of glial proteins than wild-type mice. These findings suggest that leptin affects the development of glial cells. In this study, therefore, we investigated oligodendrocyte development in the cerebral cortex of ob/ob and wild-type mouse embryos by histochemistry. METHODS We obtained ob/ob or wild-type (C57BL/6J) embryos on embryonic day (E) 18. We performed immunohistochemistry in the embryonic cerebrum with antibodies against NG2, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and leptin receptor (Ob-R). In the cerebral cortex, we compared the number of the oligodendrocyte precursor cells (OPCs), which are immunopositive for NG2 and/or PDGFR-alpha, between ob/ob and wild-type embryos. RESULTS We revealed that ob/ob embryos had significantly more OPCs than wild-type embryos on E18. PDGFR-alpha-positive OPCs did not coexpress leptin receptor in the cerebral cortex. CONCLUSION These findings suggest that leptin inhibits differentiation of multipotent and/or glial progenitor cells into OPCs in the mouse embryonic cerebral cortex, but it does not directly act on OPCs.