Lorber Barbara, Berry Martin, Logan Ann, Tonge David
Department of Medicine, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom.
Mol Cell Neurosci. 2002 Oct;21(2):301-11. doi: 10.1006/mcne.2002.1175.
Recent studies have shown that lens lesion promotes axonal regeneration in the optic nerve of adult rats. In the present investigations, dissociated retinal ganglion cells (RGC) from intact postnatal (P) 9-11 rats showed spontaneous neurite outgrowth on laminin-1, in contrast to RGC from intact P14-adult rats. Neurite outgrowth from P9-14 RGC on laminin-1 was promoted by prior lens lesion and also during coculture with lesioned lenses. Neurite outgrowth from adult RGC following prior lens lesion, or in cocultures with lesioned lenses, required the presence of laminin-2. In media conditioned by lesioned lenses, the stimulatory effect on neurite outgrowth was still observed in the presence of K252a (trk receptor blocker) and mAb 228 (which blocks the effects of leukemia inhibitory factor and ciliary neurotrophic factor). Together, these results suggest the existence of a neuritogenic factor(s) associated with the lesioned lens that belongs to neither the neurotrophin nor the gp130 cytokine family.
最近的研究表明，晶状体损伤可促进成年大鼠视神经中的轴突再生。在本研究中，与出生后（P）14天至成年大鼠的视网膜神经节细胞（RGC）不同，出生后第9至11天完整大鼠的解离RGC在层粘连蛋白-1上显示出自发性神经突生长。层粘连蛋白-1上P9至14 RGC的神经突生长可通过先前的晶状体损伤以及与损伤晶状体共培养来促进。先前晶状体损伤后或与损伤晶状体共培养时成年RGC的神经突生长需要层粘连蛋白-2的存在。在损伤晶状体条件培养基中，在存在K252a（trk受体阻滞剂）和单克隆抗体228（其阻断白血病抑制因子和睫状神经营养因子的作用）的情况下，仍观察到对神经突生长的刺激作用。总之，这些结果表明存在一种与损伤晶状体相关的神经突生长因子，它既不属于神经营养因子家族也不属于gp130细胞因子家族。
