Distinct effects of p75 in mediating actions of neurotrophins on basal forebrain oligodendrocytes

Du, Yangzhou; Fischer, Tanya; Clinton-Luke, Patricia; Lercher, Lauren D.; Dreyfus, Cheryl F.

doi:10.1016/j.mcn.2005.11.001

Cited by 49 publications

(59 citation statements)

References 57 publications

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“…Alternatively, our findings could be explained if LINGO-1 in trans was directly suppressing another inductive signal. For instance, BDNF can induce oligodendrocyte differentiation via TrkB (28), and there is evidence that, at least in retinal ganglion cells, LINGO-1 can interact with TrkB to inhibit phosphorylation induced by BDNF (11). We find this mechanism less likely to explain our present observations for two reasons.…”

Section: Discussionmentioning

confidence: 58%

LINGO-1, a Transmembrane Signaling Protein, Inhibits Oligodendrocyte Differentiation and Myelination through Intercellular Self-interactions

Jepson

Vought

Gross

et al. 2012

Journal of Biological Chemistry

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Background: Myelination of axons by oligodendrocytes is critical for neuronal function. LINGO-1, a cell receptor, inhibits myelination. Results: An extracellular fragment of LINGO-1 binds to LINGO-1 displayed on a cell surface and also inhibits oligodendrocyte maturation and myelination. Conclusion: LINGO-1 in axons and oligodendrocytes can self-interact to inhibit myelination. Significance: Understanding mechanisms governing myelination may lead to the treatment of demyelinating diseases like multiple sclerosis.

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Section: Discussionmentioning

confidence: 58%

LINGO-1, a Transmembrane Signaling Protein, Inhibits Oligodendrocyte Differentiation and Myelination through Intercellular Self-interactions

Jepson

Vought

Gross

et al. 2012

Journal of Biological Chemistry

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“…The effects of p75 NTR blockade on bladder function in control (no inflammation) and CYP-treated rats (48 h) were evaluated by immunoneutralization with intravesical infusion of anti-p75 NTR monoclonal antibody (ATS; 100 g/ml) or PD90780 (Pfizer; 10 -100 M), known to specifically block NGF-p75 NTR (14,22,55,69) using conscious cystometry (continuous fill and isovolumetric). Immediately before cystometric analysis, rats were anesthetized (1-2% isoflurane) and bladders were manually emptied with the Credé maneuver.…”

Section: Drug Treatmentsmentioning

confidence: 99%

“…Rats were then infused (Յ1 ml) with either anti-p75 NTR monoclonal antibody (n ϭ 9) or with PD90780 (n ϭ 24) maintained (30 min) in the bladder while the rat was anesthetized (isoflurane, 1-2%) to prevent voiding and expulsion of bladder contents (7,15). The concentrations and duration of PD90780 infusion chosen for this study were based on previous experiments with PD90780 (14,22,55,69). The concentration antip75 NTR monoclonal antibody used for intravesical infusion was based on previous studies using anti-p75 NTR or anti-NGF in intrathecal infusion or cell culture applications (22,36,47,52,53).…”

Section: Drug Treatmentsmentioning

confidence: 99%

Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Klinger

Vizzard²

2008

American Journal of Physiology-Renal Physiology

106

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NTR in bladder function in control and CYP-treated rats was determined using conscious cystometry and immunoneutralization or PD90780, a compound known to specifically block NGF binding to p75NTR . An anti-p75 NTR monoclonal antibody or PD90780 was infused intravesically and cystometric parameters were evaluated. Both methods of p75 NTR blockade significantly (P Յ 0.05) decreased the intercontraction interval and void volume in control and CYP-treated rats. Intravesical infusion of PD90780 also significantly (P Յ 0.001) increased intravesical pressure and increased the number of nonvoiding contractions during the filling phase. Control intravesical infusions of isotype-matched IgG and vehicle were without effect. Intravesical instillation of PD90780 significantly (P Յ 0.01) reduced the volume threshold to elicit a micturition contraction in control rats (no inflammation) and CYP-treated in a closed urinary bladder system. These studies demonstrate 1) ubiquitous p75 NTR expression in urinary bladder and increased expression with CYP-induced cystitis and 2) p75 NTR blockade at the level of the urinary bladder produces bladder hyperreflexia in control and CYP-treated rats. The overall activity of the urinary bladder reflects the balance of NGF-p75 NTR and NGF-TrkA signaling. NTR belongs to the tumor necrosis factor-␣ family of receptors (1, 4, 8). p75 NTR binds all neurotrophins, including brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4/5. NGF-TrkA signaling is involved in some inflammatory effects of NGF (50), including sensitization of nociceptive afferents and the release of neuropeptides. TrkA expression is increased in bladder afferent cells in lumbosacral dorsal root ganglia (DRG) with acute and chronic cyclophosphamide (CYP)-induced bladder inflammation (51). In addition, p75 NTR expression is also significantly upregulated in bladder afferent cells (2.4-to 2.8-fold) in lumbosacral DRG after CYP-induced cystitis (39).The pan-neurotrophin receptor p75 NTR exhibits a ubiquitous distribution and has many functions and multiple binding partners and ligands (4,8). In the absence of Trk expression, p75NTR is suggested to be involved in apoptosis and regulation of neuronal growth (4, 27); however, in the presence of TrkA, p75 NTR is suggested to function by enhancing Trk binding to neurotrophins (3,4,70). p75 NTR expression has previously been identified in the urinary bladder (61,66,67) but few studies have examined the role of p75 NTR in bladder function or in the context of urinary bladder inflammation (66). Although we do know that p75NTR expression is present in micturition reflex pathways in control rats and is regulated with CYP-induced cystitis (39), the potential role(s) of p75 NTR in urinary bladder reflexes have not been explored. In this study, we determined 1) expression of p75 NTR in the urinary bladder with immunohistochemistry and Western blot and regulation of p75 NTR expression after CYP-induced cystitis, 2) the effect of immunoneutralization with an anti-p75 NTR monoc...

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“…The lessons learned for optimizing remyelination from endogenous cycling cells may also provide important insights to improve remyelination from transplanted cells, which may also be limited by characteristics of the chronically demyelinated lesion environment [56]. An important future challenge will be to not only promote remyelination of viable denuded axons but also to integrate neurotrophic factors, such as BDNF, in order to enhance regeneration of damaged or transected axons to accomplish more extensive recovery [57][58][59].…”

Section: Future Perspectivementioning

confidence: 99%

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

Armstrong

2007

Future Neurol.

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Remyelination facilitates recovery of saltatory conduction along demyelinated axons and may help prevent axon damage in patients with demyelinating diseases, such as multiple sclerosis. The extent of remyelination in multiple sclerosis lesions varies dramatically, indicating a capacity for repair that is not fulfilled in lesions with poor remyelination. In experimental models of demyelinating disease, remyelination is limited by chronic disease that depletes the oligodendrocyte progenitor (OP) population, inhibits OP differentiation into remyelinating oligodendrocytes and/or perturbs cell survival in the lesion environment. Manipulating the activity of growth factor signaling pathways significantly improves the ability of endogenous OP cells to accomplish extensive remyelination. Specifically, growth factors have been identified that can regulate OP proliferation, differentiation and survival in demyelinated lesions. Therefore, growth factors may be key signals for strategies to improve conditions with poor remyelination. Keywords cuprizone; demyelinating disease; FGF; multiple sclerosis; myelin; oligodendrocyte; PDGF; progenitors; remyelination Transition to in vivo analysis during remyelinationAnalysis of growth factors to promote repair in demyelinating diseases has undergone an important transition to in vivo studies and in doing so has revealed much more than the expected results. Characterization of the bipotential oligodendrocyte-type 2 astrocyte or oligodendrocyte progenitor (OP) cell, and the regulation of cell fate by serum components [1] opened the door for in vitro analysis of growth factor responses in the oligodendrocyte lineage. Numerous subsequent in vitro studies identified specific growth factors capable of regulating differentiation, proliferation, migration and survival at specific stages within this lineage. In vitro studies continue to offer distinct advantages for isolating molecular and cellular mechanisms of action and for characterizing the potential of defined growth factors to induce a specific cellular response. In this context, several cytokines and chemokines have been identified as having direct effects on oligodendrocyte lineage cells that are similar to growth factor actions and so they will be discussed together under the rubric of growth factors. This review will focus on recent in vivo remyelination studies designed to test potential growth factor responses identified in vitro. These in vivo studies demonstrate important effects of growth factors in the context of demyelinating disease models in rodents. However, not all growth factor analyses have resulted in the predicted responses. Importantly, several studies have demonstrated a remarkable capacity of endogenous cells to repair the adult CNS, even following chronic demyelination, using modulation of growth factor signaling to better support oligodendrocyte replacement and myelin formation.

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Distinct effects of p75 in mediating actions of neurotrophins on basal forebrain oligodendrocytes

Cited by 49 publications

References 57 publications

LINGO-1, a Transmembrane Signaling Protein, Inhibits Oligodendrocyte Differentiation and Myelination through Intercellular Self-interactions

LINGO-1, a Transmembrane Signaling Protein, Inhibits Oligodendrocyte Differentiation and Myelination through Intercellular Self-interactions

Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

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Distinct effects of p75 in mediating actions of neurotrophins on basal forebrain oligodendrocytes

Cited by 49 publications

References 57 publications

LINGO-1, a Transmembrane Signaling Protein, Inhibits Oligodendrocyte Differentiation and Myelination through Intercellular Self-interactions

LINGO-1, a Transmembrane Signaling Protein, Inhibits Oligodendrocyte Differentiation and Myelination through Intercellular Self-interactions

Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

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Role of p75^NTR in female rat urinary bladder with cyclophosphamide-induced cystitis