Trophic factors and neuronal survival

Barde, Yves‐Alain

doi:10.1016/0896-6273(89)90040-8

Cited by 1,559 publications

(704 citation statements)

References 103 publications

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“…Neuronal growth and survival are being influ enced by a range of peptide growth factors (Barde, 1989), but only few may have neuroprotective prop erties, too. Some growth factors may also be able to stimulate cellular repair mechanisms, which can lead to functional recovery.…”

Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor-β₁Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Prehn

Backhauß

Krieglstein

1993

J Cereb Blood Flow Metab

223

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Transforming growth factor-β1 (TGF-β1) has been shown to be an injury-related peptide growth factor within the mammalian central nervous system. We tested whether TGF-β1 has the capacity to protect rat neocortical neurons against excitotoxic damage in vitro and mouse neocortex against ischemic injury in vivo. After 14 days in vitro, cultured neurons from rat cerebral cortex were exposed to 1 m M l-glutamate in serum-free culture medium. The cultures received TGF-β1 immediately after the addition of glutamate. Eighteen hours later, the cell viability of the cultures was determined using trypan blue exclusion. TGF-β1 (1–10 ng/ml) significantly reduced the excitotoxic neuronal damage in a concentration-dependent manner. In vivo, male NMRI mice were subjected to a permanent occlusion of the left middle cerebral artery by microbipolar electrocoagulation. After 48 h, the animals received a transcardiac injection of carbon black. The area of ischemia (devoid of carbon) was restricted to the neocortex and its size was determined planimetrically by means of an image-analyzing system. The treatment with TGF-β1 (1 μg/kg i.c.v.) at 6, 4, or 2 h prior to vessel occlusion reduced the area of ischemia by 5.3, 10.0, and 9.6%, respectively. The effect of the treatment with TGF-β1 was statistically significant (p < 0.05 by two-way ANOVA). The present in vitro and in vivo data suggest that TGF-β1 has the capacity to diminish the deleterious consequences of an excitotoxic or ischemic insult.

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Section: Discussionmentioning

confidence: 99%

Transforming Growth Factor-β₁Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Prehn

Backhauß

Krieglstein

1993

J Cereb Blood Flow Metab

223

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“…At the time of target ®eld innervation, sympathetic and sensory neurons become dependent on target-derived nerve growth factor (NGF) (Levi-Montalcini, 1987;Barde, 1989;Ra et al, 1993). NGF action is mediated by two classes of cell surface receptors: TrkA Klein et al, 1991), a member of the Trk family of tyrosine kinase receptors and the low a nity receptor p75 NTR (Johnson et al, 1986) that, besides binding NGF, binds the other neurotrophins as well (Rodriguez-Tebar et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Induction of apoptosis by p75 neurotrophin receptor in human neuroblastoma cells

et al. 1997

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The low-a nity nerve growth factor receptor p75 NTR belongs to a membrane receptor superfamily whose members, in certain cell types, are able to transduce an apoptotic signal. To investigate the e ect of p75 NTR expression in neuroblastoma cells, we transfected the p75 NTR cDNA into SK-N-BE cells, a neuroblastoma cell line that lacks expression of both p75 NTR and TrkA. Cell clones expressing elevated levels of p75 NTR showed a high degree of cell death by apoptosis, even in serumsupplemented medium. Moreover, the level of apoptosis correlated directly with the expression level of the receptor, indicating that p75 NTR could activate the cell death program by itself. Clones expressing p75 NTR showed a dramatic increase of cell death when switched into serum-free medium; these cultures rapidly extinguished. This apoptotic e ect was greatly inhibited by NGF treatment. Our results support the hypothesis that p75 NTR , when it is not bound by NGF, may play a role in neuronal selection during embryonic development and suggest that neuroblastomas may arise from immature neuroblasts that escape programmed cell death. Therefore, the loss of p75 NTR expression in developing neural crest cells might be a primary event in the genesis of neuroblastoma.

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“…Conversely, the implantation of an additional extremity anlage resulted in an increase of the number of motoneurons projecting into the augmented target area (31,37). The further extension and evaluation of this concept, replacing the physiological target of motoneurons by sarcoma tissue, resulted-by a cascade of lucky coincidences-in the discovery of nerve growth factor (NGF) (summarized in 48), the molecular incarnation of the retrograde trophic influence of peripheral target cells on sympathetic and subpopulations of sensory (both neural crest and placode derived) neurons (summarized in 4,48,104).…”

Section: Introductionmentioning

confidence: 99%

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

Thoenen¹,

Hughes²,

Sendtner³

1993

Experimental Neurology

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Trophic factors and neuronal survival

Cited by 1,559 publications

References 103 publications

Transforming Growth Factor-β₁Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Transforming Growth Factor-β₁Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Induction of apoptosis by p75 neurotrophin receptor in human neuroblastoma cells

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

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Trophic factors and neuronal survival

Cited by 1,559 publications

References 103 publications

Transforming Growth Factor-β1Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Transforming Growth Factor-β1Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Induction of apoptosis by p75 neurotrophin receptor in human neuroblastoma cells

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

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Transforming Growth Factor-β₁Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo

Transforming Growth Factor-β₁Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo