Seiwa Chika, Nakahara Jin, Komiyama Takatsugu, Katsu Yoshinao, Iguchi Taisen, Asou Hiroaki
Glial Cell Research Group, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
Neuroendocrinology. 2004;80(1):21-30. doi: 10.1159/000080663.
We report studies on the mechanism of action of bisphenol A (BPA) on the differentiation of oligodendrocyte precursor cells (OPCs). Our results show that: (1) BPA inhibits the differentiation of OPCs induced by exposure to thyroid hormone (T3). (2) The effect is mediated through various mechanisms via the thyroid hormone receptor (TRbeta1) which is considered to be responsible for OPC differentiation. (3) The action of BPA on OPC differentiation does not involve the FcRgamma-Fyn-myelin basic protein (MBP) cascade as an inducer of OPC differentiation nor does it suppress CREB phosphorylation, which is considered to be induced by the T3-TR complex. (4) The presence of MBP isoforms (21.5, 18.5, 17.0 and 14.0 kDa) was detected in OPCs, and the expression of exon 2-containing isoforms (i.e. 17.0 and 21.5 kDa) was upregulated upon treatment with T3. In contrast, expression of MBP was inhibited by BPA.
我们报告了关于双酚A（BPA）对少突胶质前体细胞（OPCs）分化作用机制的研究。我们的结果表明：（1）BPA抑制暴露于甲状腺激素（T3）诱导的OPCs分化。（2）该效应通过甲状腺激素受体（TRbeta1）经由多种机制介导，TRbeta1被认为对OPCs分化负责。（3）BPA对OPCs分化的作用不涉及作为OPCs分化诱导剂的FcRgamma - Fyn - 髓鞘碱性蛋白（MBP）级联反应，也不抑制被认为由T3 - TR复合物诱导的CREB磷酸化。（4）在OPCs中检测到MBP亚型（21.5、18.5、17.0和14.0 kDa）的存在，并且用T3处理后含第2外显子的亚型（即17.0和21.5 kDa）的表达上调。相反，MBP的表达被BPA抑制。
