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Rat retinal ganglion cells upregulate the pro-apoptotic BH3-only protein Bim after optic nerve transection

Näpänkangas, Ulla; Lindqvist, Niclas LU ; Lindholm, Dan and Hallböök, Finn (2003) In Molecular Brain Research 120(1). p.30-37
Abstract

Increased expression of Bim, a pro-apoptotic member of the Bcl-2 family, has been shown to be critical for neuronal apoptosis. To study the involvement of Bim in injury-induced cell death in retina, Bim expression was studied in normal rat retina and in retina after optic nerve transection using quantitative RT-PCR and immunohistochemistry. As a complement to this, the apoptotic regulators Bax, Bcl-2, caspase-3 and phosphorylated c-jun were studied. The relative levels of Bim mRNA in retina were significantly higher 4 days after optic nerve transection and below normal levels at 14 days after transection. A parallel increase in the number of Bim-immunoreactive cells in the retinal ganglion cell layer could be seen. Bim-immunoreactivity... (More)

Increased expression of Bim, a pro-apoptotic member of the Bcl-2 family, has been shown to be critical for neuronal apoptosis. To study the involvement of Bim in injury-induced cell death in retina, Bim expression was studied in normal rat retina and in retina after optic nerve transection using quantitative RT-PCR and immunohistochemistry. As a complement to this, the apoptotic regulators Bax, Bcl-2, caspase-3 and phosphorylated c-jun were studied. The relative levels of Bim mRNA in retina were significantly higher 4 days after optic nerve transection and below normal levels at 14 days after transection. A parallel increase in the number of Bim-immunoreactive cells in the retinal ganglion cell layer could be seen. Bim-immunoreactivity localized to retrogradely True Blue-labeled retinal ganglion cells. The relative mRNA levels for both Bax and Bcl-2 were higher at 4 days after transection when compared to normal. Immunoreactivity for Bax, Bcl-2 as well as for caspase-3 and phosphorylated c-jun, indicative of cell death, localized to True Blue-identified retinal ganglion cells 4 days after injury. Bcl-2 immunoreactivity was also seen on other cells, most likely Müller glia cells. In addition, optic nerve transection caused an increase in Bim, Bax, and Bcl-2 mRNA levels in optic nerve and superior colliculus. Our results suggest that Bim is involved in injury-induced retinal ganglion cell death and indicate that the increase in Bim and Bax expression promote cell death of axotomized retinal ganglion cells whereas the elevation in Bcl-2 in retina may contribute to the control of the extent of apoptosis after the optic nerve transection. © 2003 Elsevier B.V. All rights reserved.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
Apoptosis, Axotomy, Cell death, MRNA, Optic nerve
in
Molecular Brain Research
volume
120
issue
1
pages
8 pages
publisher
Elsevier
external identifiers
  • scopus:0344304804
ISSN
0169-328X
DOI
10.1016/j.molbrainres.2003.09.016
language
English
LU publication?
no
id
878d64e2-ac3e-40cd-bfd8-6fbca42964e6
date added to LUP
2017-06-02 15:18:34
date last changed
2017-06-25 05:02:32
@article{878d64e2-ac3e-40cd-bfd8-6fbca42964e6,
  abstract     = {<p>Increased expression of Bim, a pro-apoptotic member of the Bcl-2 family, has been shown to be critical for neuronal apoptosis. To study the involvement of Bim in injury-induced cell death in retina, Bim expression was studied in normal rat retina and in retina after optic nerve transection using quantitative RT-PCR and immunohistochemistry. As a complement to this, the apoptotic regulators Bax, Bcl-2, caspase-3 and phosphorylated c-jun were studied. The relative levels of Bim mRNA in retina were significantly higher 4 days after optic nerve transection and below normal levels at 14 days after transection. A parallel increase in the number of Bim-immunoreactive cells in the retinal ganglion cell layer could be seen. Bim-immunoreactivity localized to retrogradely True Blue-labeled retinal ganglion cells. The relative mRNA levels for both Bax and Bcl-2 were higher at 4 days after transection when compared to normal. Immunoreactivity for Bax, Bcl-2 as well as for caspase-3 and phosphorylated c-jun, indicative of cell death, localized to True Blue-identified retinal ganglion cells 4 days after injury. Bcl-2 immunoreactivity was also seen on other cells, most likely Müller glia cells. In addition, optic nerve transection caused an increase in Bim, Bax, and Bcl-2 mRNA levels in optic nerve and superior colliculus. Our results suggest that Bim is involved in injury-induced retinal ganglion cell death and indicate that the increase in Bim and Bax expression promote cell death of axotomized retinal ganglion cells whereas the elevation in Bcl-2 in retina may contribute to the control of the extent of apoptosis after the optic nerve transection. © 2003 Elsevier B.V. All rights reserved.</p>},
  author       = {Näpänkangas, Ulla and Lindqvist, Niclas and Lindholm, Dan and Hallböök, Finn},
  issn         = {0169-328X},
  keyword      = {Apoptosis,Axotomy,Cell death,MRNA,Optic nerve},
  language     = {eng},
  month        = {12},
  number       = {1},
  pages        = {30--37},
  publisher    = {Elsevier},
  series       = {Molecular Brain Research},
  title        = {Rat retinal ganglion cells upregulate the pro-apoptotic BH3-only protein Bim after optic nerve transection},
  url          = {http://dx.doi.org/10.1016/j.molbrainres.2003.09.016},
  volume       = {120},
  year         = {2003},
}