کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956834 | 1099459 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Receptor protein tyrosine phosphatase sigma inhibits axon regrowth in the adult injured CNS
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Recently, receptor protein tyrosine phosphatase-Ï (RPTPÏ) has been shown to inhibit axon regeneration in injured peripheral nerves. Unlike the peripheral nervous system (PNS), central nervous system (CNS) neurons fail to regenerate their axons after injury or in disease. In order to assess the role of RPTPÏ in CNS regeneration, we used the retinocollicular system of adult mice lacking RPTPÏ to evaluate retinal ganglion cell (RGC) axon regrowth after optic nerve lesion. Quantitative analysis demonstrated a significant increase in the number of RGC axons that crossed the glial scar and extended distally in optic nerves from RPTPÏ (â/â) mice compared to wild-type littermate controls. Although we found that RPTPÏ is expressed by adult RGCs in wild-type mice, the retinas and optic nerves of adult RPTPÏ (â/â) mice showed no histological defects. Furthermore, the time-course of RGC death after nerve lesion was not different between knockout and wild-type animals. Thus, enhanced axon regrowth in the absence of RPTPÏ could not be attributed to developmental defects or increased neuronal survival. Finally, we show constitutively elevated activity of mitogen-activated protein kinase (MAPK) and Akt kinase in adult RPTPÏ (â/â) mice retinas, suggesting that these signaling pathways may contribute to promoting RGC axon regrowth following traumatic nerve injury. Our results support a model in which RPTPÏ inhibits axon regeneration in the adult injured CNS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 28, Issue 4, April 2005, Pages 625-635
Journal: Molecular and Cellular Neuroscience - Volume 28, Issue 4, April 2005, Pages 625-635
نویسندگان
Przemyslaw S. Sapieha, Laure Duplan, Noriko Uetani, Sandrine Joly, Michel L. Tremblay, Timothy E. Kennedy, Adriana Di Polo,