【摘 要】
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The inability of retinal ganglion cells (RGCs) to regenerate their axons after optic nerve damage has dire consequences for victims of traumatic or ischemic nerve damage or glaucoma.In animal models o
【机 构】
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Boston Children's Hospital and Harvard Medical School, Boston, MA, USA
【出 处】
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第三届国际神经再生高峰论坛暨第五届脊髓损伤治疗与临床试验国际交流会(INRS2013 & 5th ISCITT)
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The inability of retinal ganglion cells (RGCs) to regenerate their axons after optic nerve damage has dire consequences for victims of traumatic or ischemic nerve damage or glaucoma.In animal models of optic nerve injury,regenerative failure can be partially reversed by reactivating RGCs intrinsic growth state.One way to accomplish this goal is by inducing a limited inflammatory reaction in the eye,which causes neutrophils and macrophages to enter the eye and secrete oncomodulin (Ocm).Ocm is an atypical growth factor that binds to RGCs in a cAMP-dependent fashion and activates downstream signaling cascades that lead to considerable axon growth (Yin et al.,2006; Yin et al.,2009).An alternative way to promote regeneration is by deleting the gene for PTEN,a suppressor of signaling through the PI3 kinase pathway (Park et al.,2008).Combining pten deletion in RGCs with elevation of Ocm and cAMP induces 10 times more long-distance regeneration than any of these alone (Kurimoto et al.,2010).After 10-12 weeks,this treatment enables some RGCs to regenerate axons the full length of the optic nerve,across the chiasm,and into the di- and mesencephalon,where they form synapses in the LGN,superior colliculus and other visual target areas.Regeneration leads to a partial recovery of the optomotor response,depth avoidance,and entrainment of circadian activity to the ambient day-night cycle (de Lima ef al.,2012).We are currently investigating methods to augment RGC survival and axon regeneration beyond current levels,and developing ways to translate these findings into gene-therapy approaches that can be used in patients with optic nerve damage.
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