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Sternberg,C.; Benchimol,M.; Linden,R.. |
We examined the degeneration of post-mitotic ganglion cells in ex-vivo neonatal retinal explants following axon damage. Ultrastructural features of both apoptosis and autophagy were detected. Degenerating cells reacted with antibodies specific for activated caspase-3 or -9, consistent with the presence of caspase activity. Furthermore, peptidic inhibitors of caspase-9, -6 or -3 prevented cell death (100 µM Ac-LEDH-CHO, 50 µM Ac-VEID-CHO and 10 µM Z-DEVD-fmk, respectively). Interestingly, inhibition of autophagy by 7-10 mM 3-methyl-adenine increased the rate of cell death. Immunohistochemistry data, caspase activation and caspase inhibition data suggest that axotomy of neonatal retinal ganglion cells triggers the intrinsic apoptotic pathway, which, in turn,... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Apoptosis; Autophagy; Caspases; Retina; Central nervous system. |
Ano: 2010 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2010001000005 |
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Linden,R.; Chiarini,L.B.. |
Programmed cell death in the form of apoptosis involves a network of metabolic events and may be triggered by a variety of stimuli in distinct cells. The nervous system contains several neuron and glial cell types, and developmental events are strongly dependent on selective cell interactions. Retinal explants have been used as a model to investigate apoptosis in nervous tissue. This preparation maintains the structural complexity and cell interactions similar to the retina in situ, and contains cells in all stages of development. We review the finding of nuclear exclusion of several transcription factors during apoptosis in retinal cells. The data reviewed in this paper suggest a link between apoptosis and a failure in the nucleo-cytoplasmic partition of... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Programmed cell death; Retina; Neurogenesis; Development; Nuclear membrane. |
Ano: 1999 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000700003 |
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