Lam Joyce Shi-Ying, Wang Liqing, Lin Ling, Chan Sun-On
Department of Anatomy, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China.
Neurosci Lett. 2008 Mar 21;434(1):150-4. doi: 10.1016/j.neulet.2008.01.064. Epub 2008 Feb 6.
Chondroitin sulfate proteoglycans elicit a selective inhibition to neurite growth from ventrotemporal (VT) but not dorsonasal (DN) retina, potentiating the bilateral routing of axons in the mouse optic chiasm. We examined whether this selective response is mediated by a difference in protein kinase C (PKC) expression. Effects of suppressing PKC activity in explant preparations of embryonic day 14 retinae with inhibitor Gö6976 or Ro-32-0432 abolished the chondroitin sulfate inhibition to the VT neurites but had no effect to the DN neurites. Whether these responses rely on a difference in expression of PKC in the growth cones was examined using antibodies against six isozymes of PKC. Among these the alpha, betaI and epsilon isozymes were expressed prominently in the retinal growth cones; whilst the betaII, delta and gamma isozymes were barely detected. Moreover, while the alpha and epsilon isozymes were abundant in the filopodial and lamellipodial processes, the betaI isozyme was restricted largely in the core region of the growth cones. Despite these subtype specific localization, there was no significant difference in expression of any of these PKC isozymes between growth cones from VT and DN retina, indicating that the selective response to chondroitin sulfates is not likely generated by a regulation of PKC expression, but by expression of surface molecules that interact with chondroitin sulfate proteoglycans.
硫酸软骨素蛋白聚糖对来自颞腹侧(VT)而非鼻背侧(DN)视网膜的神经突生长产生选择性抑制,增强了小鼠视交叉中轴突的双侧路径。我们研究了这种选择性反应是否由蛋白激酶C(PKC)表达的差异介导。用抑制剂Gö6976或Ro - 32 - 0432抑制胚胎第14天视网膜外植体制备物中的PKC活性,消除了硫酸软骨素对VT神经突的抑制作用,但对DN神经突没有影响。使用针对PKC六种同工酶的抗体研究了这些反应是否依赖于生长锥中PKC表达的差异。其中,α、βI和ε同工酶在视网膜生长锥中显著表达;而βII、δ和γ同工酶几乎未被检测到。此外,虽然α和ε同工酶在丝状伪足和片状伪足过程中丰富,但βI同工酶主要局限于生长锥的核心区域。尽管有这些亚型特异性定位,但VT和DN视网膜生长锥之间这些PKC同工酶的表达没有显著差异,这表明对硫酸软骨素的选择性反应不太可能由PKC表达的调节产生,而是由与硫酸软骨素蛋白聚糖相互作用的表面分子的表达产生。