PTEN deletion enhances the regenerative ability of adult corticospinal neurons
نویسندگان
چکیده
منابع مشابه
Short hairpin RNA against PTEN enhances regenerative growth of corticospinal tract axons after spinal cord injury.
Developing approaches to promote the regeneration of descending supraspinal axons represents an ideal strategy for rebuilding neuronal circuits to improve functional recovery after spinal cord injury (SCI). Our previous studies demonstrated that genetic deletion of phosphatase and tensin homolog (PTEN) in mouse corticospinal neurons reactivates their regenerative capacity, resulting in signific...
متن کاملPten deletion in adult neural stem/progenitor cells enhances constitutive neurogenesis.
Here we show that conditional deletion of Pten in a subpopulation of adult neural stem cells in the subependymal zone (SEZ) leads to persistently enhanced neural stem cell self-renewal without sign of exhaustion. These Pten null SEZ-born neural stem cells and progenies can follow the endogenous migration, differentiation, and integration pathways and contribute to constitutive neurogenesis in t...
متن کاملRestoration of skilled locomotion by sprouting corticospinal axons induced by co-deletion of PTEN and SOCS3.
The limited rewiring of the corticospinal tract (CST) only partially compensates the lost functions after stroke, brain trauma and spinal cord injury. Therefore it is important to develop new therapies to enhance the compensatory circuitry mediated by spared CST axons. Here by using a unilateral pyramidotomy model, we find that deletion of cortical suppressor of cytokine signaling 3 (SOCS3), a ...
متن کاملPten Deletion Promotes Regrowth of Corticospinal Tract Axons 1 Year after Spinal Cord Injury.
UNLABELLED Chronic spinal cord injury (SCI) is a formidable hurdle that prevents a large number of injured axons from crossing the lesion, particularly the corticospinal tract (CST). This study shows that Pten deletion in the adult mouse cortex enhances compensatory sprouting of uninjured CST axons. Furthermore, forced upregulation of mammalian target of rapamycin (mTOR) initiated either 1 mont...
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ژورنال
عنوان ژورنال: Nature Neuroscience
سال: 2010
ISSN: 1097-6256,1546-1726
DOI: 10.1038/nn.2603