Nadarajah B, Makarenkova H, Becker D L, Evans W H, Parnavelas J G
Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom.
J Neurosci. 1998 Oct 1;18(19):7881-90. doi: 10.1523/JNEUROSCI.18-19-07881.1998.
We have found that basic fibroblast growth factor (bFGF), applied to cortical progenitor cells in vitro, produces an increase in the expression of the gap junction protein connexin (Cx) 43 and in the mRNA encoding Cx 43. This effect was evident in both proliferating and nonproliferating cells. The elevated levels of mRNA suggest that bFGF is likely to exert its effect by upregulating the rate of transcription of the Cx 43 gene. We have further shown that the increase in Cx 43 expression is mediated through the receptor tyrosine kinase pathway and is associated with enhanced intercellular dye-coupling mediated by gap junctions. These results suggest that gap junction channels provide a direct conduit for mitogens released in response to bFGF to effectively regulate proliferation during corticogenesis.
我们发现，体外应用于皮质祖细胞的碱性成纤维细胞生长因子（bFGF）可使缝隙连接蛋白连接蛋白（Cx）43的表达以及编码Cx 43的mRNA增加。这种效应在增殖细胞和非增殖细胞中均很明显。mRNA水平的升高表明，bFGF可能通过上调Cx 43基因的转录速率发挥其作用。我们进一步表明，Cx 43表达的增加是通过受体酪氨酸激酶途径介导的，并且与缝隙连接介导的细胞间染料偶联增强有关。这些结果表明，缝隙连接通道为响应bFGF释放的促有丝分裂原提供了一条直接途径，以在皮质发生过程中有效调节增殖。
