Cytokine Regulation of Photoreceptor Gene Expression

神经性细胞因子在预防或延缓失明方面显示出巨大的治疗潜力。 其中几种细胞因子刺激gp130受体。任何一种白血病抑制因子的刺激 睫状神经营养因子(CNTF)或LiF对视网膜细胞有三种深刻的影响：抑制 分化；对视网膜退化的神经保护；以及光感受器的光反应减弱。 尽管人们对这些影响感兴趣，但对gp130在正常视网膜发育或 它在防止光感受器死亡方面的作用。在这项研究中，我们将使用组织特异性的gp130失活来 回答三个重要的问题。1.gp130在视网膜正常分化中起什么作用？ 光感受器或Muller细胞中gp130的表达是否与神经保护和功能有关？ 丢失？3.PI3K/Akt通路是否参与gp130诱导的神经保护？

Neurological cytokines have shown tremendous therapeutic potential for preventing or delaying blindness. Several of these cytokines stimulate the receptor gp130. Stimulation with either leukemia inhibitory factor (LIF) or ciliary neurotrophic factor (CNTF) has three profound effects on retinal cells: inhibition of differentiation; neuroprotection from retinal degeneration; and reduced light response of photoreceptors. Despite the interest in these effects, little is known about the role of gp130 in normal retinal development or its role in preventing photoreceptor death. In this study we will use tissue specific inactivation of gp130 to address three important questions. 1.What is the role gp130 in normal differentiation of the retina? 2. Is gp130 expression in photoreceptors or Muller cells responsible for neuroprotection and function loss? 3. Is the PI3K/Akt pathway responsible for gp130 induced neuroprotection?