Transcriptional regulation of Trk family neurotrophin receptors

Le, Lei; Parada, Luis F.

doi:10.1007/s00018-006-6328-8

Cited by 36 publications

(22 citation statements)

References 112 publications

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“…This might be due to the time and location dependent regulation of the Trk receptors, influencing the effectiveness of the neurotrophins [72,73]. …”

Section: Discussionmentioning

confidence: 99%

Interleukin-1 beta and neurotrophin-3 synergistically promote neurite growth in vitro

Boato

Hechler

Rosenberger

et al. 2011

J Neuroinflammation

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Pro-inflammatory cytokines such as interleukin-1 beta (IL-1β) are considered to exert detrimental effects during brain trauma and in neurodegenerative disorders. Consistently, it has been demonstrated that IL-1β suppresses neurotrophin-mediated neuronal cell survival rendering neurons vulnerable to degeneration. Since neurotrophins are also well known to strongly influence axonal plasticity, we investigated here whether IL-1β has a similar negative impact on neurite growth. We analyzed neurite density and length of organotypic brain and spinal cord slice cultures under the influence of the neurotrophins NGF, BDNF, NT-3 and NT-4. In brain slices, only NT-3 significantly promoted neurite density and length. Surprisingly, a similar increase of neurite growth was induced by IL-1β. Additionally, both factors increased the number of brain slices displaying maximal neurite growth. Furthermore, the co-administration of IL-1β and NT-3 significantly increased the number of brain slices displaying maximal neurite growth compared to single treatments. These data indicate that these two factors synergistically stimulate two distinct aspects of neurite outgrowth, namely neurite density and neurite length from acute organotypic brain slices.

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“…This might be due to the time and location dependent regulation of the Trk receptors, influencing the effectiveness of the neurotrophins [72,73]. …”

Section: Discussionmentioning

confidence: 99%

Interleukin-1 beta and neurotrophin-3 synergistically promote neurite growth in vitro

Boato

Hechler

Rosenberger

et al. 2011

J Neuroinflammation

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“…5 In contrast, the precise role of p75NTR has been slow to emerge. Recent findings suggest that p75NTR contributes to different signaling pathways.…”

mentioning

confidence: 99%

p75 neurotrophin receptor mediates apoptosis in transit-amplifying cells and its overexpression restores cell death in psoriatic keratinocytes

et al. 2010

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p75 neurotrophin receptor (p75NTR) belongs to the TNF-receptor superfamily and signals apoptosis in many cell settings. In human epidermis, p75NTR is mostly confined to the transit-amplifying (TA) sub-population of basal keratinocytes. Brainderived neurotrophic factor (BDNF) or neurotrophin-4 (NT-4), which signals through p75NTR, induces keratinocyte apoptosis, whereas b-amyloid, a ligand for p75NTR, triggers caspase-3 activation to a greater extent in p75NTR transfected cells. Moreover, p75NTR co-immunoprecipitates with NRAGE, induces the phosphorylation of c-Jun N-terminal kinase (JNK) and reduces nuclear factor kappa B (NF-jB) DNA-binding activity. p75NTR also mediates pro-NGF-induced keratinocyte apoptosis through its co-receptor sortilin. Furthermore, BDNF or b-amyloid cause cell death in TA, but not in keratinocyte stem cells (KSCs) or in p75NTR silenced TA cells. p75NTR is absent in lesional psoriatic skin and p75NTR levels are significantly lower in psoriatic than in normal TA keratinocytes. The rate of apoptosis in psoriatic TA cells is significantly lower than in normal TA cells. BDNF or b-amyloid fail to induce apoptosis in psoriatic TA cells, and p75NTR retroviral infection restores BDNF-or b-amyloid-induced apoptosis in psoriatic keratinocytes. These results demonstrate that p75NTR has a pro-apoptotic role in keratinocytes and is involved in the maintenance of epidermal homeostasis.

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“…P75 NTR is downregulated in the adult (with exceptions) but can be upregulated under pathological conditions (Dechant and Barde 2002;Blöchl and Blöchl 2007). The molecular mechanisms that control the cellspecific expression pattern of Trks and p75 NTR await further elucidation (Lei and Parada 2007). P75 NTR can interact not only with Trks but also with sortilin, LINGO-1, and NogoR (Mi et al 2004;Lu et al 2005;Nykjaer et al 2005).…”

Section: Neurotrophins and Their Receptorsmentioning

confidence: 98%

Oligodendroglial Cells and Neurotrophins: A Polyphonic Cantata in Major and Minor

et al. 2008

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Oligodendrocytes met neurotrophins in the early 1990s of the last century. Since then, their relationship underwent functional ups and downs partially dependent on the developmental stage of the oligodendroglial cells and the species, from which the cells were derived. This review provides a brief overview of oligodendroglial cells and neurotrophins, characterizes neurotrophin signaling during oligodendroglial development, and discusses the significance of proneurotrophins and sortilin for oligodendroglial death and survival. Furthermore, data are provided that TrkA, the tyrosine kinase competent NGF receptor, is localized to caveolincontaining microdomains on the oligodendroglial plasma membrane; an interplay of caveolin and NGF signaling via TrkA might be of functional importance. Finally, experimental evidence of studies is presented which support the idea that neurotrophins are promising candidates for improving oligodendroglial regeneration and remyelination.

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Transcriptional regulation of Trk family neurotrophin receptors

Cited by 36 publications

References 112 publications

Interleukin-1 beta and neurotrophin-3 synergistically promote neurite growth in vitro

Interleukin-1 beta and neurotrophin-3 synergistically promote neurite growth in vitro

p75 neurotrophin receptor mediates apoptosis in transit-amplifying cells and its overexpression restores cell death in psoriatic keratinocytes

Oligodendroglial Cells and Neurotrophins: A Polyphonic Cantata in Major and Minor

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