کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956901 | 1099463 | 2005 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury](/preview/png/10956901.png)
چکیده انگلیسی
Axon growth after spinal injury is thought to be limited in part by myelin-derived proteins that act via the Nogo-66 Receptor (NgR). To test this hypothesis, we sought to study recovery from spinal cord injury (SCI) after inhibiting NgR transgenically with a soluble function-blocking NgR fragment. Glial fibrillary acidic protein (gfap) gene regulatory elements were used to generate mice that secrete NgR(310)ecto from astrocytes. After mid-thoracic dorsal over-hemisection injury, gfapâ·ngr(310)ecto mice exhibit enhanced raphespinal and corticospinal axonal sprouting into the lumbar spinal cord. Recovery of locomotion is improved in the gfapâ·ngr(310)ecto mice. These data indicate that the NgR ligands, Nogo-66, MAG, and OMgp, play a role in limiting axonal growth in the injured adult CNS and that NgR(310)ecto might provide a therapeutic means to promote recovery from SCI.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 29, Issue 1, May 2005, Pages 26-39
Journal: Molecular and Cellular Neuroscience - Volume 29, Issue 1, May 2005, Pages 26-39
نویسندگان
Shuxin Li, Ji-Eun Kim, Stephane Budel, Thomas G. Hampton, Stephen M. Strittmatter,