MURINE OLIGODENDROGLIAL CELLS EXPRESS NERVE GROWTH-FACTOR

MURINE OLIGODENDROGLIAL CELLS EXPRESS NERVE GROWTH-FACTOR
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DOI:
10.1073/pnas.91.19.8812
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发表时间:
1994-09-13
影响因子:
11.1
通讯作者:
CAMPAGNONI, AT
CAMPAGNONI, AT
中科院分区:
综合性期刊1区
文献类型:
--
作者:
BYRAVAN, S;FOSTER, LM;CAMPAGNONI, AT

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这里报道的研究提出的证据表明,神经生长因子(NGF)和脑源性神经营养因子(BDNF)的表达的少突胶质细胞系和神经生长因子的少突胶质细胞在小鼠原代培养。表达未成熟少突胶质细胞标记物的永生化少突胶质细胞系(N19)刺激PC 12细胞进行精细加工。简并引物聚合酶链反应分析表明,N19细胞表达神经营养因子NGF和BDNF的mRNA。北方印迹分析证实N19细胞表达1.3-kb的NGF mRNA和1.4-kb和4-kb的BDNF mRNA。原位杂交组织化学鉴定了9天的原代少突胶质细胞培养中存在的NGF mRNA。结合免疫细胞化学和原位杂交组织化学共定位NGFmRNA在原代培养告诉免疫染色的少突胶质细胞标志物半乳糖苷(GC)。双重免疫荧光分析也在GC(+)细胞和A(2)B(5)+细胞(少突胶质细胞祖细胞的标志物)内共定位NGF蛋白。这些结果表明,少突胶质细胞及其前体细胞可以表达神经营养因子NGF。他们认为少突胶质细胞谱系中的细胞除了髓鞘形成外,还可能在通过纤维束的神经突延伸中发挥积极作用。
The studies reported here present evidence for the expression of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) by an oligodendroglial cell line and of NGF by oligodendrocytes in mouse primary culture. An immortalized oligodendroglial cell line (N19) expressing markers for immature oligodendrocytes stimulated PC12 cells to elaborate processes. Polymerase chain reaction analysis with degenerate primers indicated that the N19 cells expressed the mRNAs for the neurotrophic factors NGF and BDNF. Northern blot analysis confirmed that the N19 cells expressed the 1.3-kb NGF mRNA and the 1.4- and 4-kb BDNF mRNAs. In situ hybridization histochemistry identified the presence of NGF mRNAs in 9-day primary oligodendroglial cultures. Combined immunocytochemistry and in situ hybridization histochemistry colocalized NGF mRNA within primary cultured tells that immunostained for the oligodendrocyte marker galactocerebroside (GC). Double-immunofluorescence analysis also colocalized NGF protein within GC(+) cells and within A(2)B(5)+ cells, a marker for oligodendrocyte progenitors. These results show that oligodendroglia and their precursor cells can express the neurotrophic factor NGF. They suggest that cells in the oligodendrocyte lineage may play an active role in neurite extension through fiber tracts in addition to myelination.