Literature DB >> 10321489

Retinal ganglion cell loss after the period of naturally occurring cell death in bcl-2-/- mice.

A Cellerino1, T Michaelidis, J J Barski, M Bähr, H Thoenen, M Meyer.   

Abstract

Over-expression of Bcl-2 is known to reduce the extent of retinal ganglion cell death during development as well as after axotomy. Here we investigated whether retinal ganglion cell (RGC) numbers are reduced in mice with a targeted inactivation of the bcl-2 gene. Compared with wild-type mice, adult bcl-2 null mutants have lost 29% of the retinal ganglion cell axons in the optic nerve. This reduction was almost fully established at P15, but not present at P10, which marks the end of the period of naturally occurring cell death. These observations, together with the previously reported late loss of primary motoneurons and peripheral neurons, point to a general physiological requirement for Bcl-2 soon after the period of naturally occurring cell death.

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Year:  1999        PMID: 10321489     DOI: 10.1097/00001756-199904060-00034

Source DB:  PubMed          Journal:  Neuroreport        ISSN: 0959-4965            Impact factor:   1.837


  3 in total

1.  Targeted disruption of the bcl-2 gene in mice exacerbates focal ischemic brain injury.

Authors:  R Hata; F Gillardon; T M Michaelidis; K A Hossmann
Journal:  Metab Brain Dis       Date:  1999-06       Impact factor: 3.584

2.  BCL2L1 (BCL-X) promotes survival of adult and developing retinal ganglion cells.

Authors:  Jeffrey M Harder; Qian Ding; Kimberly A Fernandes; Jonathan D Cherry; Lin Gan; Richard T Libby
Journal:  Mol Cell Neurosci       Date:  2012-07-24       Impact factor: 4.314

3.  BBC3 (PUMA) regulates developmental apoptosis but not axonal injury induced death in the retina.

Authors:  Jeffrey M Harder; Richard T Libby
Journal:  Mol Neurodegener       Date:  2011-07-15       Impact factor: 14.195

  3 in total

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