Cholera toxin regulates a signaling pathway critical for the expansion of neural stem cell cultures from the fetal and adult rodent brains.
Cholera toxin regulates a signaling pathway critical for the expansion of neural stem cell cultures from the fetal and adult rodent brains.
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DOI：
10.1371/journal.pone.0010841
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发表时间：
2010-05-26
期刊：
影响因子：
3.7
通讯作者：
McKay RD
中科院分区：
文献类型：
--
作者：
Androutsellis-Theotokis A;Walbridge S;Park DM;Lonser RR;McKay RD
调节神经干细胞(NSC)扩张的新机制将有助于改进检测系统和针对内源性干细胞的新兴再生方法。扩大关于干细胞自我更新控制的知识也将导致针对癌症干细胞群体的新方法。在这里，我们发现霍乱毒素调节两个最近表征的神经干细胞标志物，Tie2受体和转录因子Hes3，并促进培养的NSCs的扩增。霍乱毒素增加Tie2受体的免疫反应性，并迅速诱导Hes3的核定位。紧随其后的是强大的培养神经干细胞扩增和在有丝分裂原存在和不存在的情况下诱导增殖。我们的数据表明了一种新的细胞生物学机制，它调节干细胞的自我更新和分化特性，为在再生疾病和癌症的背景下操纵神经干细胞提供了新的逻辑。
New mechanisms that regulate neural stem cell (NSC) expansion will contribute to improved assay systems and the emerging regenerative approach that targets endogenous stem cells. Expanding knowledge on the control of stem cell self renewal will also lead to new approaches for targeting the stem cell population of cancers. Here we show that Cholera toxin regulates two recently characterized NSC markers, the Tie2 receptor and the transcription factor Hes3, and promotes the expansion of NSCs in culture. Cholera toxin increases immunoreactivity for the Tie2 receptor and rapidly induces the nuclear localization of Hes3. This is followed by powerful cultured NSC expansion and induction of proliferation both in the presence and absence of mitogen. Our data suggest a new cell biological mechanism that regulates the self renewal and differentiation properties of stem cells, providing a new logic to manipulate NSCs in the context of regenerative disease and cancer.
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