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大鼠星形胶质细胞中的离子反应与生长刺激:神经节苷脂和血清的不同作用机制

Ionic responses and growth stimulation in rat astroglial cells: differential mechanisms of gangliosides and serum.

作者信息

Skaper S D, Varon S

出版信息

J Cell Physiol. 1987 Mar;130(3):453-9. doi: 10.1002/jcp.1041300320.

DOI:10.1002/jcp.1041300320
PMID:3558496
Abstract

Rat astroglial cells respond to fetal calf serum (FCS) and gangliosides, including GM1, by undergoing proliferation. Here, we show that addition of FCS but not GM1 causes an increase in Na+, K+-pump activity, as measured by ouabain-sensitive 86Rb+ influx. The increase of Na+, K+-pump activity by FCS was due to increased Na+ influx (measured with 22Na+). This increased Na+ influx was sensitive to amiloride, an inhibitor of Na+/H+ exchange. Amiloride also blocked the FCS-stimulated incorporation of [3H]thymidine into DNA. Two defined polypeptide growth factors, epidermal growth factor and fibroblast growth factor were also able to elicit an amiloride-sensitive Na+ influx and an ouabain-sensitive K+ uptake in these astroglial cells, in the presence of FCS or insulin. Thus, GM1 differs from serum and growth factors in the mechanisms by which these agents stimulate the proliferation of the astroglial cells used here.

摘要

大鼠星形胶质细胞通过增殖对胎牛血清(FCS)和神经节苷脂(包括GM1)作出反应。在此,我们表明添加FCS而非GM1会导致钠钾泵活性增加,这是通过哇巴因敏感的86Rb+内流来测量的。FCS引起的钠钾泵活性增加是由于钠内流增加(用22Na+测量)。这种增加的钠内流对钠氢交换抑制剂氨氯地平敏感。氨氯地平也阻断了FCS刺激的[3H]胸腺嘧啶核苷掺入DNA。在存在FCS或胰岛素的情况下,两种确定的多肽生长因子,即表皮生长因子和成纤维细胞生长因子,也能够在这些星形胶质细胞中引发氨氯地平敏感的钠内流和哇巴因敏感的钾摄取。因此,GM1在刺激此处所用星形胶质细胞增殖的机制上与血清和生长因子不同。

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Ionic responses and growth stimulation in rat astroglial cells: differential mechanisms of gangliosides and serum.大鼠星形胶质细胞中的离子反应与生长刺激:神经节苷脂和血清的不同作用机制
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A role for gangliosides in astroglial cell differentiation in vitro.神经节苷脂在体外星形胶质细胞分化中的作用。
J Cell Biol. 1988 Mar;106(3):821-8. doi: 10.1083/jcb.106.3.821.
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Exogenously administered gangliosides fail to increase in vivo metastatic frequency or in vitro growth of murine neoplastic cells.外源性给予的神经节苷脂未能增加小鼠肿瘤细胞的体内转移频率或体外生长。
Clin Exp Metastasis. 1990 Mar-Apr;8(2):181-92. doi: 10.1007/BF00117791.