The low-affinity p75 receptor for nerve growth factor (p75NGFR) has been implicated in mediating neuronal cell death in vitro. A recent in vitro study from our laboratory showed that the death of sensory neurons can be prevented by reducing the levels of p75NGFR with antisense oligonucleotides. To d
Level of p75 receptor expression in sensory ganglia is modulated by NGF level in the target tissue
✍ Scribed by Kitzman, Patrick H. ;Perrone, Teresa N. ;LeMaster, Ann M. ;Davis, Brian M. ;Albers, Kathryn M.
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 390 KB
- Volume
- 35
- Category
- Article
- ISSN
- 0022-3034
No coin nor oath required. For personal study only.
✦ Synopsis
Neurotrophins play an essential role in sensory development by providing trophic support to neurons that innervate peripheral targets. Nerve growth factor (NGF), neurotrophin-3, neurotrophin-4, and brain-derived neurotrophin exert their survival effect by binding to two transmembrane receptor types: trk receptors, which exhibit binding specificity, and the p75NTR receptor, which binds all neurotrophins. To determine how target-derived neurotrophins affect sensory neuron development and function, we used transgenic mice that overexpress NGF in the skin to examine the impact of NGF overexpression on receptor expression. Previous studies of trk expression in trigeminal ganglia of adult NGF transgenics showed that the percentage of trkA neurons doubled and their number increased fivefold. The present study focused on the p75 receptor and shows that the percentage of neurons expressing p75NTR also increase in NGF ganglia, but only by 10%. This increase did not encompass the small, BS-IB-4 isolectin-positive cells as they remained p75 negative in transgenic ganglia. Interestingly, levels of trkA protein were not increased on a per-cell level, whereas levels of p75NTR increased nearly threefold. These results show that in sensory systems, target-derived NGF modulates the level of p75NTR receptor expression, and in so doing, may act to regulate the formation of functional receptor complexes and subsequent trophic action.
📜 SIMILAR VOLUMES
## Abstract Neurotrophin‐3 (NT‐3) can negatively modulate trkA and associated phenotype in intact sensory neurons, while positively regulating trkC and associated phenotype. How NT‐3 effects this response is not clear. Whether NT‐3 exerts a differential influence on levels of activated ERK1/2 signa
## Abstract Precursor cells have the capacity to repopulate the demyelinated brain, but the molecular mechanisms that facilitate their recruitment are largely unknown. The low‐affinity neurotrophin receptor, p75^NTR^, may be one of these regulators; however, its expression profile by oligodendrogli
## Abstract ZEB1 and SNAIL repress __CDH1__ and induce epithelial–mesenchymal transition (EMT). However, SNAIL and ZEB1 also activate or regulate other target genes in different ways. For instance, vitamin D receptor (VDR), which activates __CDH1__ expression upon ligand binding, is repressed by SN
High expression of the epidermal growth factor receptor (EGFR) in breast carcinoma confers a growth advantage to the tumor cells. The EGFR tyrosine kinase inhibitor (EGFR-TKI) ZD1839 ('Iressa') has clinical activity in a wide range of tumor types, although the mechanism(s) by which it exerts its ant
Matrix metalloproteinase-1 (MMP-1) is one of only a few enzymes with the ability to degrade the stromal collagens (types I and III) at neutral pH, and high expression of MMP-1 has been associated with aggressive and invasive cancers. We recently reported a single nucleotide insertion/deletion polymo