Axonal regeneration of optic nerve after crush in Nogo66 receptor knockout mice.
نویسندگان
چکیده
Mature retinal ganglion cells (RGCs) cannot regenerate injured axons because some neurite growth inhibitors, including the C-terminal of Nogo-A (Nogo66), myelin-associated glycoprotein (MAG) and Omgp, exert their effects on neuron regeneration through the Nogo receptor (NgR). In this study, the axonal regeneration of retinal ganglion cells (RGCs) after optic nerve (ON) crush was investigated both in vivo and in vitro in NgR knockout mice. We used NgR knockout mice as the experimental group, and C57BL/6 mice as the control group. Partial ON injury was induced by using a specially designed ON clip to pinch the ON 1mm behind the mouse eyeball with 40g pressure for 9s. NgR mRNA was studied by in situ hybridization (ISH). NgR protein was studied by Western blot. Growth Associated Protein 43 (GAP-43), a plasticity protein expressed highly during axon regeneration, was studied by immunofluorescence staining on the frozen sections. RGCs were cultured and purified. The axonal growth of RGCs was calculated by a computerized image analyzer. We found that compared with the control group, the GAP-43 expression was significantly higher and the axonal growth was significantly more active at every observation time point in the experimental group. These results indicate that NgR genes play an important role in the axonal regeneration after ON injury, while knockout of NgR is effective for eliminating this inhibition and enhancing axonal regeneration.
منابع مشابه
Axonal regeneration after optic nerve crush in Nogo-A/B/C knockout mice
PURPOSE The axonal regeneration of retinal ganglion cells (RGCs) after optic nerve (ON) crush was investigated both in vivo and in vitro on Nogo-A/B/C knockout mice. METHODS The study used 20 Nogo-A/B/C knockout mice in the experimental group, and 20 C57BL/6 mice in the control group. Partial ON injury was induced by using a specially designed ON clip to pinch the ON 1 mm behind the mouse eye...
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ورودعنوان ژورنال:
- Neuroscience letters
دوره 460 3 شماره
صفحات -
تاریخ انتشار 2009