Proshin Sergey, Yamaguchi Kazunori, Wada Tadashi, Miyagi Taeko
Division of Biochemistry, Research Institute of Miyagi Prefectural Cancer Center, Natori, Japan.
Neurochem Res. 2002 Aug;27(7-8):841-6. doi: 10.1023/a:1020269326825.
Plasma membrane-associated sialidase (Neu 3), which specifically hydrolyzes gangliosides, is relatively abundantly present in the nervous system. To understand the role of Neu 3 in neuronal differentiation, we studied the relationship between neurite outgrowth and Neu 3 expression in human neuroblastoma NB-1 cells. The expression of Neu 3 in NB-1 cells increased when neurite outgrowth in these cells was induced by dibutyryl cAMP. While treatment with dibutyryl cAMP alone enhanced the outgrowth of dendrite-like processes, transfection of the Neu 3 gave rise to a more prominent outgrowth of neurites with axon-like characteristics, even in the absence of dibutyryl cAMP. Neu 3 induction by dibutyryl cAMP is probably attributable, in part, to transactivation of the Neu 3 gene through cAMP responsive elements in the 5'-upstream region, as revealed by the promotor activity assay using Neu 3 promotor expression plasmid. These results indicate that Neu 3 regulates neurite formation in NB-1 cells, and suggest that this effect may be enhanced by dibutyryl cAMP via a cAMP-dependent pathway.
质膜相关唾液酸酶（Neu 3）能特异性水解神经节苷脂，在神经系统中相对大量存在。为了解Neu 3在神经元分化中的作用，我们研究了人神经母细胞瘤NB - 1细胞中神经突生长与Neu 3表达之间的关系。当用二丁酰环磷腺苷（dibutyryl cAMP）诱导NB - 1细胞的神经突生长时，这些细胞中Neu 3的表达增加。单独用二丁酰环磷腺苷处理可增强树突样突起的生长，而Neu 3的转染即使在没有二丁酰环磷腺苷的情况下也会导致具有轴突样特征的神经突更显著地生长。如使用Neu 3启动子表达质粒进行的启动子活性测定所示，二丁酰环磷腺苷对Neu 3的诱导可能部分归因于通过5'上游区域的环磷腺苷反应元件对Neu 3基因的反式激活。这些结果表明Neu 3调节NB - 1细胞中的神经突形成，并提示二丁酰环磷腺苷可能通过环磷腺苷依赖性途径增强这种作用。
