Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-11-12
pubmed:abstractText
The extracellular matrix protein fibronectin is implicated in neuronal regeneration in the peripheral nervous system. In the central nervous system (CNS), fibronectin is up-regulated at sites of penetrating injuries and stroke; however, CNS neurons down-regulate the fibronectin receptor alpha5beta1 integrin during differentiation and generally respond poorly to fibronectin. NT2N CNS neuron-like cells (derived from NT2 precursor cells) have been used in preclinical and clinical studies for treatment of stroke and a variety of CNS injury and disease models. Here we show that, like primary CNS neurons, NT2N cells down-regulate alpha5beta1 integrin during differentiation and respond poorly to fibronectin. The poor neurite outgrowth by NT2N cells on fibronectin can be rescued by transducing NT2 precursors with a retroviral vector expressing alpha5 integrin under the control of the murine stem cell virus 5' long terminal repeat. Sustained alpha5 integrin expression is compatible with the CNS-like neuronal differentiation of NT2N cells and does not prevent robust neurite outgrowth on other integrin ligands. Thus, alpha5 integrin expression in CNS neuronal precursor cells may provide a strategy for enhancing the outgrowth and survival of implanted cells in cell-replacement therapies for CNS injury and disease.
pubmed:grant
pubmed:commentsCorrections
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pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1097-4547
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
222-32
pubmed:dateRevised
2011-7-19
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Expression of alpha5 integrin rescues fibronectin responsiveness in NT2N CNS neuronal cells.
pubmed:affiliation
Department of Biology, University of Iowa, Iowa City, Iowa, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural