ArticleCell death & disease2013
Suppression of SHP-1 promotes corticospinal tract sprouting and functional recovery after brain injury.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Experience-driven competition in neural reorganization after stroke.The Journal of physiology · 2025Review
- Inhibition of HDAC increases BDNF expression and promotes neuronal rewiring and functional recovery after brain injury.Cell death & disease · 2020Article
- Differential expression of genes involved in the acute innate immune response to intracortical microelectrodes.Acta biomaterialia · 2020Article
- MARCKSL1 Regulates Spine Formation in the Amygdala and Controls the Hypothalamic-Pituitary-Adrenal Axis and Anxiety-Like Behaviors.EBioMedicine · 2018Article
- Motor compensation and its effects on neural reorganization after stroke.Nature reviews. Neuroscience · 2017Review
- Tamoxifen and Src kinase inhibitors as neuroprotective/neuroregenerative drugs after spinal cord injury.Neural regeneration research · 2015Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reorganization of spared neural network connections is one of the most important processes for restoring impaired function after brain injury. However, plasticity is quite limited in the adult brain due to the presence of inhibitory molecules and a lack of intrinsic neuronal signals for axonal growth. Src homology 2-containing phosphatase (SHP)-1 has been shown to have a role in axon growth inhibition. Here, we tested the hypothesis that SHP-1 negatively affects axonal reorganization. We observed that unilateral motor cortex injury led to increased expression and activity of SHP-1 in the contralesional cortex. In this model, corticospinal axons originating from the contralesional cortex sprouted into the denervated side of the cervical spinal cord after injury. We observed that the number of sprouting fibers was increased in SHP-1-deficient heterozygous viable motheaten (+/me(v)) mice, which show reduced SHP-1 activity, and in wild-type mice treated with an SHP inhibitor. Motor function recovery of impaired forelimb was enhanced in +/me(v) mice. Collectively, our results indicate that downregulation of SHP-1 activity promotes corticospinal tract sprouting and functional recovery after brain injury.
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Registered trials
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