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Neuronal myosin-X is upregulated after peripheral nerve injury and mediates laminin-induced growth of neurites
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
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2013 (English)In: Molecular and Cellular Neuroscience, ISSN 1044-7431, E-ISSN 1095-9327, Vol. 56, 96-101 p.Article in journal (Refereed) Published
Abstract [en]

The successful outcome of peripheral neuronal regeneration is attributed both to the growth permissive milieu and the intrinsic ability of the neuron to initiate appropriate cellular responses such as changes in gene expression and cytoskeletal rearrangements. Even though numerous studies have shown the importance of interactions between the neuron and the extracellular matrix (ECM) in axonal outgrowth, the molecular mechanisms underlying the contact between ECM receptors and the cellular cytoskeleton remain largely unknown. Unconventional myosins constitute an important group of cytoskeletal-associated motor proteins. One member of this family is the recently described myosin-X. This protein interacts with several members of the axon growth-associated ECM receptor family of integrins and could therefore be important in neuronal outgrowth. In this study, using radioactive in situ hybridization, we found that expression of myosin-X mRNA is upregulated in adult rat sensory neurons and spinal motoneurons after peripheral nerve injury, but not after central injury. Thus, myosin-X was upregulated after injuries that can-be followed by axonal regeneration. We also found that the protein is localized to neuronal growth cones and that silencing of myosin-X using RNA interference impairs the integrin-mediated growth of neurites on laminin, but has no effect on non-integrin mediated growth on N-cadherin.

Place, publisher, year, edition, pages
2013. Vol. 56, 96-101 p.
Keyword [en]
Extracellular matrix, axon regeneration, peripheral neuron, cell culture, lesion models
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-210739DOI: 10.1016/j.mcn.2013.04.001ISI: 000325834100010OAI: oai:DiVA.org:uu-210739DiVA: diva2:664276
Available from: 2013-11-14 Created: 2013-11-14 Last updated: 2013-11-14Bibliographically approved

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