Adult Neuronal Regeneration Induced by Transgenic Integrin Expression

In a variety of adult CNS injury models, embryonic neurons exhibit superior regenerative performance when compared with adult neurons. It is unknown how young neurons extend axons in the injured adult brain, in which adult neurons fail to regenerate. This study shows that cultured adult neurons do n...

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Bibliographic Details
Published in:The Journal of neuroscience 2001-07, Vol.21 (13), p.4782-4788
Main Author: Condic, Maureen L
Format: Article
Language:English
Subjects:
Adenoviridae - genetics
Aging - metabolism
Animals
Animals, Newborn
Cell Division - drug effects
Cell Division - genetics
Cells, Cultured
Fibronectins - metabolism
Fibronectins - pharmacology
Ganglia, Spinal - cytology
Ganglia, Spinal - metabolism
Gene Expression
Integrin alpha1beta1
Integrins - biosynthesis
Integrins - genetics
Laminin - metabolism
Laminin - pharmacology
Ligands
Nerve Regeneration - drug effects
Nerve Regeneration - genetics
Neurons, Afferent - cytology
Neurons, Afferent - drug effects
Neurons, Afferent - metabolism
Rats
Receptors, Fibronectin - biosynthesis
Receptors, Fibronectin - genetics
Transfection
Transgenes
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Summary:In a variety of adult CNS injury models, embryonic neurons exhibit superior regenerative performance when compared with adult neurons. It is unknown how young neurons extend axons in the injured adult brain, in which adult neurons fail to regenerate. This study shows that cultured adult neurons do not adapt to conditions that are characteristic of the injured adult CNS: low levels of growth-promoting molecules and the presence of inhibitory proteoglycans. In contrast, young neurons readily adapt to these same conditions, and adaptation is accompanied by an increase in the expression of receptors for growth-promoting molecules (receptors of the integrin family). Surprisingly, the regenerative performance of adult neurons can be restored to that of young neurons by gene transfer-mediated expression of a single alpha-integrin.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.21-13-04782.2001