The subcellular distribution of transferrin in rat choroid plexus studied with immunogold labelling of ultracryosections. Histochem J
Department A, Panum Institute, University of Copenhagen, Denmark. The Histochemical Journal
09/1989; 21(8):441-8. DOI: 10.1007/BF01845793
Choroid plexus epithelium from third ventricle choroid plexus of 2-3-week-old rats was examined for transferrin-like immunoreactivity. In 5 microns paraffin sections most epithelial cells exhibited a pronounced immunoperoxidase staining for transferrin. The ultrastructure of the epithelium in question was examined by conventional electron microscopy. Immunolabelling of ultracryosections with IgG-gold, protein-A gold or protein-A gold-antiprotein-A protein-A gold showed an intense labelling of the basal extracellular space. The lateral intercellular space and the luminal surface showed a more variable labelling; no labelling of the tight junction zone was seen. Intracellularly a distinct labelling of the 'uptake and disposal pathway' (the endosomal-lysosomal system) was observed, but also the synthetic machinery (rough endoplasmic reticulum, stacked Golgi membranes) showed a characteristic labelling. Thus it seems likely that both uptake and synthesis of transferrin occur in choroid plexus epithelial cells.
Available from: Carlos Spuch
- "Many studies have demonstrated the presence of proteins and mRNA for a large number of cytokines, growth factors and hormones in the choroid plexus, for example: interleukin-1β , interleukin-6 , Tumor Necrosis Factor (TNF)-α , IGF-I , NGF , IGF-II , Transforming Growth Factor (TGF)-α , TGF-β , Vascular Endothelial Growth Factor (VEGF) , transferrin , TTR [6,18], gelsolin  and vasopressin . Most of these substances have their own receptors in the choroid plexus . "
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ABSTRACT: The presence of neurotrophins and their receptors Trk family has been reported in the choroid plexus. High levels of Nerve Growth Factor (NGF), Neurotrophin-4 (NT-4) and TrkB receptor were detected, while nothing was know about p75 neurotrophin receptor (p75NTR) in the choroid plexus epithelial cells. In neurons, p75NTR receptor has a dual function: promoting survival together with TrkA in response to NGF, and inducing apoptotic signaling through p75NTR. We postulated that p75NTR may also affect the survival pathways in the choroid plexus and also undergoes regulated proteolysis with metalloproteases.
Here, we demonstrated the presence of p75NTR receptor in the choroid plexus epithelial cells. The p75NTR receptor would be involved in cell death mechanisms and in the damaged induced by amyloid beta (Aβ) in the choroid plexus and finally, we propose an essential role of p75NTR in the Aβ transcytosis through out choroid plexus barrier.
The presence analysis reveals the new localization of p75NTR in the choroid plexus and, the distribution mainly in the cytoplasm and cerebrospinal fluid (CSF) side of the epithelial cells. We propose that p75NTR receptor plays a role in the survival pathways and Aβ-induced cell death. These data suggest that p75NTR dysfunction play an important role in the pathogenesis of brain diseases. The importance and novelty of this expression expands a new role of p75NTR.
BMC Neuroscience 05/2011; 12(1):39. DOI:10.1186/1471-2202-12-39 · 2.67 Impact Factor
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ABSTRACT: The proliferative cells of the developing hippocampal fiber tract fimbria have only the potential for gliogenesis; thus the developing fimbria provides an ideal model for the study of the development and differentiation of its constituent glial cells. In the first stage of development, the fimbrial primordium can be distinguished morphologically, and during the second stage, the fimbria becomes a well-defined fiber tract. In the third stage, a divergent immunocytochemical staining pattern clearly demarcates the neuron-free fimbria from the hippocampus, where a mixed neuro- and gliogenesis occurs. The distinct expression of S-100 protein in radial glial cells is restricted to the fimbria. During the final stage of development, the ventricular lining of the fimbria will mature into an ependyma. It is suggested that the S-100-positive radial glial cells of the fimbria, which probably retain their proliferative capacity, represent a homogeneous population of precursor cells that will give rise to the glial cells of the adult fimbria. The appearance of S-100 in the fimbrial radial glial cells seems to occur coincidentally with the establishment of hippocampal commissural connections. The S-100-positive radial glial cells of the fimbria may guide and segregate populations of growing axons by providing physical and chemical cues. Thus, S-100 protein per se seems to be intimately involved in modulation and regulation of axonal growth and patterning.
Anatomy and Embryology 02/1991; 184(6):549-58. · 1.39 Impact Factor
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ABSTRACT: The development of the human fetal hippocampus and dentate gyrus has been studied immunocytochemically. The first glial cells to appear are vimentin-positive radial glial cells. A gradual transition from vimentin to glial fibrillary acidic protein (GFAP) reactivity in the radial glial cells occurs at week 8. The GFAP-positive radial glial cells transform into astrocytes from week 14. A population of small S-100-positive somata which morphologically and spatially are distinct from GFAP-positive radial glial cells and their transformed progeny, are found as early as week 9.5 in the hippocampus during the period of peak neurogenesis. The well-defined immunoreactivity of the morphologically homogenous cell subpopulation for S-100 protein, which has been used as an astrocytic marker in the adult hippocampus, indicates that astrocytes may differentiate at very early gestational ages in human fetuses. The S-100-positive astrocytes are thought to be derived from ventricular zone cells, which at the time of their appearance do not express any of the applied astrocytic markers (S-100, GFAP, vimentin). It is suggested that the S-100-positive astrocytic cell population interacts with the first incoming projection fibers, so modulating the pattern of connectivity.
Anatomy and Embryology 02/1991; 184(6):559-69. DOI:10.1007/BF00942578 · 1.39 Impact Factor
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