Major histocompatibility complex class I molecules modulate embryonic neuritogenesis and neuronal polarization.

Major histocompatibility complex class I molecules modulate embryonic neuritogenesis and neuronal polarization.
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主要的组织相容性复合物I类分子调节胚胎神经发生和神经元极化。

DOI:
10.1016/j.jneuroim.2012.03.008
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发表时间:
2012-06-15
影响因子:
3.3
通讯作者:
Kaufman DL
Kaufman DL
中科院分区:
医学4区
文献类型:
--
作者:
Bilousova T;Dang H;Xu W;Gustafson S;Jin Y;Wickramasinghe L;Won T;Bobarnac G;Middleton B;Tian J;Kaufman DL

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我们研究了胚胎野生型、主要组织相容性复合体I类(MHCI)重链缺陷(KbDb−/−)和NSE-Db(神经元MHCI表达升高)C57BL/6小鼠的培养海马神经元。KbDb−/−神经元的神经发生和极性的建立速度较慢,而NSE-Db神经元的神经突生长速度较快,初级神经突较多,且有极化加速的趋势。对ϐ2M−/−神经元、外源性ϐ2M和自MHCI单体的进一步研究表明,与其他表面分子的自由重链顺式相互作用可以促进神经细胞的发生,而与经典MHCI受体的三方MHCI相互作用可以抑制轴突的生长。与其他结果一起,MHCI似乎对神经细胞发生和突触发生有差异调节。
We studied cultured hippocampal neurons from embryonic wildtype, major histocompatibility complex class I (MHCI) heavy chain-deficient (KbDb−/−) and NSE-Db (which have elevated neuronal MHCI expression) C57BL/6 mice. KbDb−/− neurons displayed slower neuritogenesis and establishment of polarity, while NSE-Db neurons had faster neurite outgrowth, more primary neurites, and tended to have accelerated polarization. Additional studies with ϐ2M−/− neurons, exogenous ϐ2M, and a self-MHCI monomer suggest that free heavy chain cis interactions with other surface molecules can promote neuritogenesis while tripartite MHCI interactions with classical MHCI receptors can inhibit axon outgrowth. Together with the results of others, MHCI appears to differentially modulate neuritogenesis and synaptogenesis.
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