睫状神经营养因子
糖蛋白130
白血病抑制因子
细胞生物学
车站3
生物
视网膜变性
信号转导
化学
分子生物学
受体
视网膜
神经营养因子
免疫学
细胞因子
神经科学
白细胞介素6
生物化学
作者
Yumi Ueki,Srinivas Chollangi,Yun-Zheng Le,John D. Ash
标识
DOI:10.1007/978-1-4419-1399-9_75
摘要
Members of IL-6 family cytokines, such as leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF), activate the common signal-transducing receptor gp130. We and others have previously shown that application of exogenous gp130 ligands promotes photoreceptor survival in light-induced and inherited retinal degeneration in animal models. While there is strong evidence that gp130 plays an essential role in photoreceptor protection, it is not clear whether protection is cell-autonomous in photoreceptors or an effect of Müller cell activation. To investigate the role of Müller cells in gp130-mediated photoreceptor protection, we have generated conditional gp130 knockout (KO) mice in retinal Müller cells using the Cre/lox system. Western blot and immunohistochemical analyses show that in our conditional gp130 KO mice, approximately 50% Müller cells no longer respond to LIF with activation of known downstream signaling proteins, STAT3 and ERK1/2. Despite the loss of gp130 activity in many Müller cells, intravitreal injection of LIF still induced significant degree of photoreceptor protection that was comparable to normal littermates. These data suggest that Müller cell activation of gp130 is not essential for photoreceptor protection, and support the hypothesis that the protection is mediated by cell-autonomous mechanisms in photoreceptors.
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