Can lenticular factors improve the posttrauma fate of neurons?
The intraocular lens has recently been recognized as a potential source for neuroprotective and neurite-promoting activities. The lens is ontogenetically and functionally a peculiar intraocular tissue with the unique feature of performing incomplete cellular apoptosis throughout the lifetime. The ectodermally derived epithelial cells permanently divide to produce the nuclei- and organelle-free lens fibre cells that allow for the optical transparency. The underlying extremely specific physical, biochemical, metabolic and structural mechanism lead to efficient protection from photo-oxidative stress caused by exposure to short-wavelength light. The fact that fibre cells undergo incomplete apoptosis is also of crucial importance to other cellular systems. In particular, injured nerve cells such as axotomized retinal ganglion cells may profit from the apoptosis-blocking mechanisms operating within the lens fibres. In this review we first discuss some factors involved in the lens differentiation and partial apoptosis as a basic principle of long-term survival. We then present recent experimental evidence that lenticular factors also operate outside the lens, and in particular within the retina to contribute to axonal regeneration, e.g. after a trauma. In turn, factors such as GAP-43 that were thought to be exclusively expressed within nervous tissue have now also been discovered within the lenticular tissue. Experiments of the direct confrontation of lenticular epithelial and fibre cells with regenerating ganglion cell axons in vitro are presented. It is concluded that survival factors supplied by the lens might be used to facilitate survival within neuronal tissue.
Stupp
T
T
Department of Experimental Ophthalmology, School of Medicine, University Eye Hospital of Münster and Interdisciplinary Clinical Research Center (IZKF), Domagkstrasse 15, D-48149 Münster, Germany.
Thanos
S
S
D000818:Animals; D017209:Apoptosis; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002454:Cell Differentiation; D002470:Cell Survival / Q000502:physiology; D006133:Growth Substances / Q000378:metabolism*; D006801:Humans; D007908:Lens, Crystalline / Q000293:injuries* / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000502:physiology*
D015815:Cell Adhesion Molecules; D006133:Growth Substances