Protection of retinal ganglion cells and preservation of function after optic nerve lesion in bcl-2 transgenic mice.
Multicellular organisms face the necessity of removing superfluous or injured cells during normal development, tissue turn-over and in response to damaging conditions. These finalised killings occur throughout a process, commonly called programmed cell death (PCD), which is placed under strict cellular control. PCD is regulated by the products of the expression of a number of genes. This fact raises the intriguing possibility of inhibiting such degenerative processes by operating on some of the controlling genes. Central neurons of transgenic mice overexpressing bcl-2, a powerful inhibitor of PCD, are remarkably resistant to degeneration induced by noxious stimuli. We have explored the ate of retinal ganglion cells and of their axons, when such transgenic animals have been challenged by a lesion of the optic nerve. These results have direct bearing on the possibility of attaining functional restoration of the injured pathway.
Istituto di Neurofisiologia CNR, Pisa, Italy.
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Chierzi
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Maffei
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Pizzorusso
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D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis; D019771:Axotomy; D004596:Electroretinography; D019254:Genes, bcl-2 / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D009416:Nerve Regeneration; D009900:Optic Nerve / Q000502:physiology*; D010364:Pattern Recognition, Visual / Q000502:physiology; D012160:Retina / Q000502:physiology; D012165:Retinal Ganglion Cells / Q000502:physiology*