Acute neurite retraction triggered by lysophosphatidic acid: timing of the inhibitory effects of genistein.
Acute neurite retraction triggered by lysophosphatidic acid: timing of the inhibitory effects of genistein.
复制标题
溶血磷脂酸引发的急性神经突回缩：金雀异黄素抑制作用的时机。
DOI：
10.1016/0006-8993(94)91304-8
复制
发表时间：
1994
期刊：
影响因子：
2.9
通讯作者：
Ali,JY
中科院分区：
文献类型：
--
作者：
Smalheiser,NR;Ali,JY
Acute neurite retraction, elicited by diverse agents in several neuronal cell types, has been reported to be inhibited by genistein, a kinase antagonist that is relatively (though not absolutely) selective for tyrosine kinases. It was hypothesized that genistein acts upon ssome final common pathway that integrates multiple extrinsic and intrinsic signals to regulate whether neurites will execute a retraction response (J. Neurochem., 61 (1993) 340–343). To define this pathway in more detail, a quantitative study of NG108-15 cell rapid-onset neurites was carried out as they retract in response to lysophosphatidic acid (LPA, 10 μM). Following the application of LPA, most neurites exhibited early morphologic changes between 0.5 and 1.5 min, followed by progressive shortening and eventual retraction, with 50% of neurites completely retracted by 5 min and 80% gone by 10 min. Genistein did not inhibit the formation of subcortical F-actin, nor its functional competence in several assays. Genistein protected neurites when added at any time prior to the onset of the earliest morphologic changes, but failed to block progression when added to neurites that were already undergoing retraction. These findings imply that the final common pathway (i.e. the critical target(s) for genistein) must be activated late, after the increase in F-actin levels has peaked and just before retraction is initiated.
