p75 Neurotrophin Receptor Expression on Adult Human Oligodendrocytes: Signaling without Cell Death in Response to NGF

Ladiwala, Uma; Lachance, Christian; Simoneau, Steve J. J.; Bhakar, Asha L.; Barker, Philip A.; Antel, Jack P.

doi:10.1523/jneurosci.18-04-01297.1998

Cited by 128 publications

(103 citation statements)

References 41 publications

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“…The p75 receptor forms high-affinity binding sites with TrkA, and this receptor complex can lower the concentration of NGF required for signal transduction (60). Without TrkA expression, p75 can act as an inducer of apoptosis in mature rodent OLGs (61), but not in mature human OLGs (62). The cell death-inducing activity of p75 may occur through the activation of ceramide production, nuclear factor B, and c-Jun N-terminal kinase (61,63,64).…”

Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Protects Oligodendrocytes from Tumor Necrosis Factor-α-induced Injury through Akt-mediated Signaling Mechanisms

Takano¹,

Hisahara²,

Namikawa³

et al. 2000

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Protects Oligodendrocytes from Tumor Necrosis Factor-α-induced Injury through Akt-mediated Signaling Mechanisms

Takano¹,

Hisahara²,

Namikawa³

et al. 2000

Journal of Biological Chemistry

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“…Moreover, activation of NF-kB has recently been shown to occur through a pathway likewise regulated by PI3 kinase. 50 However, in other systems NF-kB activation can occur in the absence of JNK, 51 suggesting cell-type specificity.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of atypical PKC in PC12 cells enhances NGF-responsiveness and survival through an NF-κB dependent pathway

et al. 1999

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Removal of atypical PKC blocks NGF-induced differentiation of PC12 cells. 1 We now examine the consequences that overexpression of atypical PKCs had upon NGF responses. PC12 cells were stably transfected with either PKC-i or PKC-z. Overexpression of atypical PKCs markedly enhanced NGFinduced neurite outgrowth as well as enhanced NGFstimulated JNK kinase. Cotransfection of HA-JNK1 along with increasing concentrations of PKC-i, resulted in dosedependent phosphorylation of GST c-Jun (1 ± 79). NGF treatment of PC12 cells resulted in activation of NF-kB. In comparison, overexpression of atypical PKC-i was by itself sufficient to activate NF-kB and shift the kinetics of NGFinduced kB activity. Furthermore, transfection of full-length antisense PKC-i blocked basal and NGF-stimulated NF-kB. Differentiated and undifferentiated PC12 cells overexpressing atypical PKC-i were protected from serum deprivationinduced cell death. Collectively, these findings demonstrate that atypical PKC-i lies in a pathway that regulates NF-kB and contributes to both neurotrophin-mediated differentiation and survival signaling.

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“…A different picture emerges when the p75 neurotrophin receptor is present without trkA, because under these conditions NGF activates JNK and cell death can be a consequence [130,131]. Introduction of trkA removes the link to cell death [132].…”

Section: Diabetic Neuropathymentioning

confidence: 99%

Mitogen-activated protein kinases as glucose transducers for diabetic complications

1999

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The results of the Diabetes Control and Complications Trial [1] emphatically confirmed the heroic studies of Jean Pirart [2±4], showing that poor control of glycaemia in Type I (insulin-dependent) diabetes mellitus predisposes patients to chronic complications. This has led to the tacit assumption that glucose, at supranormal concentrations, is the agent of damage. Participation of hypoinsulinaemia or other manifestations of poor control cannot be discounted but glucose itself certainly has the capacity to disturb biosystems. It can do this in a variety of ways, so that hypotheses to explain specific complications ± retinopathy, nephropathy and neuropathy ± starting from high glucose are tenable, testable and, therefore, useful.Figure 1 presents a simple generic plan by which complications develop. It usefully discriminates between metabolic effects of glucose on the target cells showing the complication and the exacerbating effect of independent accelerators, such as arterial hypertension in diabetic nephropathy. Not all independent accelerators have, however, as clearly defined a rela- Diabetologia (1999) AbstractThe damaging effects of glucose on the cells which contribute to the development of diabetic complications are ill-understood. There are three major hypotheses ± the sorbitol pathway, non-enzymatic glycation of proteins and increased oxidative stress ± and many examples illustrate inter-connections between the three. It is suggested that these pathways, together with other biochemical anomalies arising from hyperglycaemia, can synergise by sharing the capacity to activate mitogen-activated protein kinases (MAP kinases) and that these enzymes in actual fact form glucose transducers. The more recent hypothesis, namely that activation of a specific isoform of protein kinase C (PKC) underpin damaging changes in retinopathy and neuropathy, can also be related because protein kinase C is an effective activator of mitogen-activated protein kinases. These latter kinases phosphorylate transcription factors, which in turn alter the balance of gene expression. In this way they can alter cellular phenotype, promote division or increase production of extracellular material. In short, mitogen-activated protein kinases have the capacity to trigger all the cellular events necessary for the development of diabetic nephropathy, retinopathy and neuropathy and it is suggested that their pharmacological modulation might provide therapeutic control of these conditions. [Diabetologia (1999

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p75 Neurotrophin Receptor Expression on Adult Human Oligodendrocytes: Signaling without Cell Death in Response to NGF

Cited by 128 publications

References 41 publications

Nerve Growth Factor Protects Oligodendrocytes from Tumor Necrosis Factor-α-induced Injury through Akt-mediated Signaling Mechanisms

Nerve Growth Factor Protects Oligodendrocytes from Tumor Necrosis Factor-α-induced Injury through Akt-mediated Signaling Mechanisms

Overexpression of atypical PKC in PC12 cells enhances NGF-responsiveness and survival through an NF-κB dependent pathway

Mitogen-activated protein kinases as glucose transducers for diabetic complications

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