A time-dependent increase in glial fibrillary acidic protein expression and glutamine synthetase activity in long-term subculture of the GL15 glioma cell line
A time-dependent increase in glial fibrillary acidic protein expression and glutamine synthetase activity in long-term subculture of the GL15 glioma cell line
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DOI：
10.1023/a:1026310905711
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发表时间：
1997-10-01
影响因子：
4
通讯作者：
Bocchini, V
中科院分区：
文献类型：
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作者：
Moretto, G;Brutti, N;Bocchini, V
1. 星形胶质细胞是中枢神经组织中数量最多的细胞成分，在生理和病理事件中发挥着关键作用。调节星形胶质细胞生长和分化的生物信号与生理学和病理学都相关，但人们对它们仍然知之甚少。 2．使用低分化胶质瘤细胞系GL15，我们研究了在长期传代培养中，这是否可以上调胶质纤维酸性蛋白（GFAP）的表达，如一些啮齿类星形胶质细胞系中所述。在相同的培养条件下，我们研究了谷氨酰胺合成酶（GS）活性、生长相关蛋白（GAP）-43表达和几种中性营养因子的表达。 3．在 GL15 细胞体外生长过程中，Western blotting 证明 GFAP 表达显着增加，长期培养中 GS 比活性也上调。 RT-PCR分析显示，GL15细胞体外停留时间不影响GAP-43、中性营养因子BDNF和NT3的表达。4．我们的结果表明，在 GL15 中，GFAP 和 GS 基因可能具有在细胞汇合时引发的共同或整合的调节机制，这可能与星形胶质细胞生理学和星形胶质细胞病理学相关。这些机制不涉及 GAP-43 和中性营养因子 BDNF 和 NT3 的表达。
1. Astrocytes are the most numerous cellular elements in the central nervous tissue, where they play a critical role in physiological and pathological events. The biological signals regulating astrocyte growth and differentiation are relevant for both physiology and pathology, but they are still little understood.2. Using a poorly differentiated glioma cell line, GL15, we investigated whether, in long-term subculture, this could upregulate the expression of glial fibrillary acidic protein (GFAP), as described in some rodent astrocyte cell lines, Under the same culture conditions, we investigated glutamine synthetase (GS) activity, growth-associated protein (GAP)-43 expression, and expression of several neutrotrophic factors.3. A dramatic increase in GFAP expression was evidenced by Western blotting during progressive in vitro growth of GL15 cells, GS specific activity was also upregulated in long-term culture. The time spent in vitro by GL15 cells did not affect GAP-43 and neutrophic factor BDNF and NT3 expression as revealed by RT-PCR analysis.4. Our results suggest that, in GL15, GFAP and GS genes may have common or integrated regulatory mechanisms elicited at the cell confluency which could be relevant for both astrocyte physiology and astrocyte pathology. These mechanisms are not involved in GAP-43 and neutrophic factor BDNF and NT3 expression.