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CNTF plus BDNF treatment and neuroprotective pathways in the rd1 mouse retina

Azadi, Seifollah LU ; Johnson, Leif LU ; Paquet-Durand, Francois LU ; Perez, Maria Thereza LU ; Zhang, Yiqin LU ; Ekström, Per LU and van Veen, Theo LU (2007) In Brain Research 1129(1). p.116-129
Abstract
The rd1 mouse is a relevant model for studying the mechanisms of photoreceptor degeneration in retinitis pigmentosa. Treatment with ciliary neurotrophic factor (CNTF) in combination with brain derived neurotrophic factor (BDNF) is known to rescue photoreceptors in cultured rd1 retinal explants. To shed light on the underlying mechanisms, we studied the effects of 9 days (starting at postnatal day 2) in vitro CNTF+BDNF treatment on the endogenous production of CNTF, BDNF, fibroblast growth factor 2 (FGF2), or the activation of extracellular signal-regulated kinase (ERK), Akt and CAMP-response-element-binding protein (CREB) in retinal explants. In rd1 explants, CNTF+BDNF decreased the number of TUNEL-positive photoreceptors. The treatment... (More)
The rd1 mouse is a relevant model for studying the mechanisms of photoreceptor degeneration in retinitis pigmentosa. Treatment with ciliary neurotrophic factor (CNTF) in combination with brain derived neurotrophic factor (BDNF) is known to rescue photoreceptors in cultured rd1 retinal explants. To shed light on the underlying mechanisms, we studied the effects of 9 days (starting at postnatal day 2) in vitro CNTF+BDNF treatment on the endogenous production of CNTF, BDNF, fibroblast growth factor 2 (FGF2), or the activation of extracellular signal-regulated kinase (ERK), Akt and CAMP-response-element-binding protein (CREB) in retinal explants. In rd1 explants, CNTF+BDNF decreased the number of TUNEL-positive photoreceptors. The treatment also increased endogenous rd1 levels of CNTF and BDNF, but lowered the level of FGF2 expression in rd1 explants. When wild-type explants were treated, endogenous CNTF was similarly increased, while BDNF and FGF2 levels remained unaffected. In addition, treatment of rd1 retinas strongly increased the phosphorylation of ERK, Akt and CREB. In treated wild-type explants, the same parameters were either unchanged (ERK) or decreased (Akt and CREB). The results suggest a role for Akt, ERK and CREB in conveying the neuroprotective effect of CNTF+BDNF treatment in rd1 retinal explants. (c) 2006 Elsevier B.V. All rights reserved. (Less)
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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
signaling, pathway, rescue, degeneration, neurotrophic factor, photoreceptor
in
Brain Research
volume
1129
issue
1
pages
116 - 129
publisher
Elsevier
external identifiers
  • wos:000243959900013
  • scopus:33846018863
ISSN
1872-6240
DOI
10.1016/j.brainres.2006.10.031
language
English
LU publication?
yes
id
0dd4c334-84b4-43c6-a691-1869b569f158 (old id 675286)
date added to LUP
2016-04-01 12:06:36
date last changed
2022-01-26 22:57:24
@article{0dd4c334-84b4-43c6-a691-1869b569f158,
  abstract     = {{The rd1 mouse is a relevant model for studying the mechanisms of photoreceptor degeneration in retinitis pigmentosa. Treatment with ciliary neurotrophic factor (CNTF) in combination with brain derived neurotrophic factor (BDNF) is known to rescue photoreceptors in cultured rd1 retinal explants. To shed light on the underlying mechanisms, we studied the effects of 9 days (starting at postnatal day 2) in vitro CNTF+BDNF treatment on the endogenous production of CNTF, BDNF, fibroblast growth factor 2 (FGF2), or the activation of extracellular signal-regulated kinase (ERK), Akt and CAMP-response-element-binding protein (CREB) in retinal explants. In rd1 explants, CNTF+BDNF decreased the number of TUNEL-positive photoreceptors. The treatment also increased endogenous rd1 levels of CNTF and BDNF, but lowered the level of FGF2 expression in rd1 explants. When wild-type explants were treated, endogenous CNTF was similarly increased, while BDNF and FGF2 levels remained unaffected. In addition, treatment of rd1 retinas strongly increased the phosphorylation of ERK, Akt and CREB. In treated wild-type explants, the same parameters were either unchanged (ERK) or decreased (Akt and CREB). The results suggest a role for Akt, ERK and CREB in conveying the neuroprotective effect of CNTF+BDNF treatment in rd1 retinal explants. (c) 2006 Elsevier B.V. All rights reserved.}},
  author       = {{Azadi, Seifollah and Johnson, Leif and Paquet-Durand, Francois and Perez, Maria Thereza and Zhang, Yiqin and Ekström, Per and van Veen, Theo}},
  issn         = {{1872-6240}},
  keywords     = {{signaling; pathway; rescue; degeneration; neurotrophic factor; photoreceptor}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{116--129}},
  publisher    = {{Elsevier}},
  series       = {{Brain Research}},
  title        = {{CNTF plus BDNF treatment and neuroprotective pathways in the rd1 mouse retina}},
  url          = {{http://dx.doi.org/10.1016/j.brainres.2006.10.031}},
  doi          = {{10.1016/j.brainres.2006.10.031}},
  volume       = {{1129}},
  year         = {{2007}},
}