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利用电穿孔技术将反义寡核苷酸选择性导入单个成年中枢神经系统祖细胞,结果表明CNTF诱导的神经胶质生成需要STAT3激活。

Selective introduction of antisense oligonucleotides into single adult CNS progenitor cells using electroporation demonstrates the requirement of STAT3 activation for CNTF-induced gliogenesis.

作者信息

Aberg M A, Ryttsén F, Hellgren G, Lindell K, Rosengren L E, MacLennan A J, Carlsson B, Orwar O, Eriksson P S

机构信息

Institute of Clinical Neuroscience, Göteborg University, SE-413 45, Sweden.

出版信息

Mol Cell Neurosci. 2001 Mar;17(3):426-43. doi: 10.1006/mcne.2000.0947.

DOI:10.1006/mcne.2000.0947
PMID:11273640
Abstract

We have developed a novel method in which antisense DNA is selectively electroporated into individual adult neural progenitor cells. By electroporation of antisense oligonucleotides against signal transducer and activator of transcription 3 (STAT3) we demonstrate that ciliary neurotrophic factor (CNTF) is an instructive signal for astroglial type 2 cell fate specifically mediated via activation of STAT3. Activation of the mitogen-activated protein kinase (MAPK) signaling pathway induced only a transient increase in glial fibrillary acidic protein (GFAP) expression, and inhibition of this signaling pathway did not block the induction by CNTF of glial differentiation in progenitor cells. In addition we show that microelectroporation is a new powerful method for introducing antisense agents into single cells in complex cellular networks.

摘要

我们开发了一种新方法,可将反义DNA选择性地电穿孔导入成年个体神经祖细胞。通过电穿孔针对信号转导和转录激活因子3(STAT3)的反义寡核苷酸,我们证明睫状神经营养因子(CNTF)是一种指导性信号,通过激活STAT3特异性介导星形胶质细胞2型细胞命运。丝裂原活化蛋白激酶(MAPK)信号通路的激活仅导致胶质纤维酸性蛋白(GFAP)表达短暂增加,抑制该信号通路并未阻断CNTF诱导祖细胞胶质分化。此外,我们表明微电穿孔是一种将反义试剂引入复杂细胞网络中单个细胞的强大新方法。

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Selective introduction of antisense oligonucleotides into single adult CNS progenitor cells using electroporation demonstrates the requirement of STAT3 activation for CNTF-induced gliogenesis.利用电穿孔技术将反义寡核苷酸选择性导入单个成年中枢神经系统祖细胞,结果表明CNTF诱导的神经胶质生成需要STAT3激活。
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