Rat retinal ganglion cells upregulate the pro-apoptotic BH3-only protein Bim after optic nerve transection
(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.
(Less)
- author
- Näpänkangas, Ulla ; Lindqvist, Niclas LU ; Lindholm, Dan and Hallböök, Finn
- publishing date
- 2003-12-12
- 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
-
- pmid:14667574
- 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
- 2024-04-14 11:56:47
@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.</p>}},
author = {{Näpänkangas, Ulla and Lindqvist, Niclas and Lindholm, Dan and Hallböök, Finn}},
issn = {{0169-328X}},
keywords = {{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}},
doi = {{10.1016/j.molbrainres.2003.09.016}},
volume = {{120}},
year = {{2003}},
}