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glial cell membrane [keywords]
- Chitosan feasibility to retain retinal stem cell phenotype and slow proliferation for retinal transplantation. [Journal Article]
- Biomed Res Int 2014.:287896.
Retinal stem cells (RSCs) are promising in cell replacement strategies for retinal diseases. RSCs can migrate, differentiate, and integrate into retina. However, RSCs transplantation needs an adequate support; chitosan membrane (ChM) could be one, which can carry RSCs with high feasibility to support their integration into retina. RSCs were isolated, evaluated for phenotype, and subsequently grown on sterilized ChM and polystyrene surface for 8 hours, 1, 4, and 11 days for analysing cell adhesion, proliferation, viability, and phenotype. Isolated RSCs expressed GFAP, PKC, isolectin, recoverin, RPE65, PAX-6, cytokeratin 8/18, and nestin proteins. They adhered (28 ± 16%, 8 hours) and proliferated (40 ± 20 cells/field, day 1 and 244 ± 100 cells/field, day 4) significantly low (P < 0.05) on ChM. However, they maintained similar viability (>95%) and phenotype (cytokeratin 8/18, PAX6, and nestin proteins expression, day 11) on both surfaces (ChM and polystyrene). RSCs did not express alpha-SMA protein on both surfaces. RSCs express proteins belonging to epithelial, glial, and neural cells, confirming that they need further stimulus to reach a final destination of differentiation that could be provided in in vivo condition. ChM does not alternate RSCs behaviour and therefore can be used as a cell carrier so that slow proliferating RSCs can migrate and integrate into retina.
- Long-Term Maintenance of Na+ Channels at Nodes of Ranvier Depends on Glial Contact Mediated by Gliomedin and NrCAM. [Journal Article]
- J Neurosci 2014 Apr 9; 34(15):5089-98.
Clustering of Na(+) channels at the nodes of Ranvier is coordinated by myelinating glia. In the peripheral nervous system, axoglial contact at the nodes is mediated by the binding of gliomedin and glial NrCAM to axonal neurofascin 186 (NF186). This interaction is crucial for the initial clustering of Na(+) channels at heminodes. As a result, it is not clear whether continued axon-glial contact at nodes of Ranvier is required to maintain these channels at the nodal axolemma. Here, we report that, in contrast to mice that lack either gliomedin or NrCAM, absence of both molecules (and hence the glial clustering signal) resulted in a gradual loss of Na(+) channels and other axonal components from the nodes, the formation of binary nodes, and dysregulation of nodal gap length. Therefore, these mice exhibit neurological abnormalities and slower nerve conduction. Disintegration of the nodes occurred in an orderly manner, starting with the disappearance of neurofascin 186, followed by the loss of Na(+) channels and ankyrin G, and then βIV spectrin, a sequence that reflects the assembly of nodes during development. Finally, the absence of gliomedin and NrCAM led to the invasion of the outermost layer of the Schwann cell membrane beyond the nodal area and the formation of paranodal-like junctions at the nodal gap. Our results reveal that axon-glial contact mediated by gliomedin, NrCAM, and NF186 not only plays a role in Na(+) channel clustering during development, but also contributes to the long-term maintenance of Na(+) channels at nodes of Ranvier.
- [Chordoid Meningioma - A Case Report: Clinicopathological Features and Differential Diagnosis of an Uncommon Tumor.] [JOURNAL ARTICLE]
- Turk Patoloji Derg 2014 Apr 9.
Meningiomas are tumors that originate from the arachnoid cell and the majority are benign and grade I tumors according to World Health Organization. Chordoid meningioma is an uncommon variant of meningioma and corresponds to grade II tumor in the World Health Organization Classification of Tumors of the Nervous System 2007 because of its more aggressive behavior and increased likelihood of recurrence. A 75-year-old female was referred to the neurosurgery department complaining of headache, syncope, and seizure. Radiological examination revealed a mass lesion in the neighbourhood of the frontal lobe that destructed bone and was associated with peritumoral edema. The patient underwent surgery. The tumor was totally excised with the dura beneath. Histopathological examination showed that the tumor was composed of clusters and cords of small polygonal cells with fine chromatin and eosinophilic vacuolated cytoplasm embedded in a myxoid matrix, and also focal whorls of spindle-shaped cells. Two mitoses were seen in 10 high power fields. Vascular proliferation was observed in some tumoral areas. Bone invasion was present. Immunohistochemical analysis of the tumor cells revealed widespread strong membranous and cytoplasmic expression of epithelial membrane antigen. The Ki67 labeling index was 6-8%. All of these findings were consistent with a diagnosis of chordoid meningioma, the neoplasm was identified as grade II based on the World Health Organization Classification, 2007. In this report we present a case of chordoid meningioma without classical radiological findings of meningioma with areas of vascular proliferation that mimicked glial tumors at histopathologic examination.
- Localization and proteomic characterization of cholesterol-rich membrane microdomains in the inner ear. [JOURNAL ARTICLE]
- J Proteomics 2014 Apr 5.
Biological membranes organize and compartmentalize cell signaling into discrete microdomains, a process that often involves stable, cholesterol-rich platforms that facilitate protein-protein interactions. Polarized cells with distinct apical and basolateral cell processes rely on such compartmentalization to maintain proper function. In the cochlea, a variety of highly polarized sensory and non-sensory cells are responsible for the early stages of sound processing in the ear, yet little is known about the mechanisms that traffic and organize signaling complexes within these cells. We sought to determine the prevalence, localization, and protein composition of cholesterol-rich lipid microdomains in the cochlea. Lipid raft components, including the scaffolding protein caveolin and the ganglioside GM1, were found in sensory, neural, and glial cells. Mass spectrometry of detergent-resistant membrane (DRM) fractions revealed over 600 putative raft proteins associated with subcellular localization, trafficking, and metabolism. Among the DRM constituents were several proteins involved in human forms of deafness including those involved in ion homeostasis, such as the potassium channel KCNQ1, the co-transporter SLC12A2, and gap junction proteins GJA1 and GJB6. The presence of caveolin in the cochlea and the abundance of proteins in cholesterol-rich DRM suggest that lipid microdomains play a significant role in cochlear physiology.Although mechanisms underlying cholesterol synthesis, homeostasis, and compartmentalization in the ear are poorly understood, there are several lines of evidence indicating that cholesterol is a key modulator of cochlear function. Depletion of cholesterol in mature sensory cells alters calcium signaling, changes excitability during development, and affects the biomechanical processes in outer hair cells that are responsible for hearing acuity. More recently, we have established that the cholesterol-modulator beta-cyclodextrin is capable of inducing significant and permanent hearing loss when delivered subcutaneously at high doses. We hypothesize that proteins involved in cochlear homeostasis and otopathology are partitioned into cholesterol-rich domains. The results of a large-scale proteomic analysis point to metabolic processes, scaffolding/trafficking, and ion homeostasis as particularly associated with cholesterol microdomains. These data offer insight into the proteins and protein families that may underlie cholesterol-mediated effects in sensory cell excitability and cyclodextrin ototoxicity.
- Investigation of a Calcium-Responsive Contrast Agent in Cellular Model Systems: Feasibility for Use as a Smart Molecular Probe in Functional MRI. [JOURNAL ARTICLE]
- ACS Chem Neurosci 2014 Apr 8.
Responsive or smart contrast agents (SCAs) represent a promising direction for development of novel functional MRI (fMRI) methods for the eventual noninvasive assessment of brain function. In particular, SCAs that respond to Ca(2+) may allow tracking neuronal activity independent of brain vasculature, thus avoiding the characteristic limitations of current fMRI techniques. Here we report an in vitro proof-of-principle study with a Ca(2+)-sensitive, Gd(3+)-based SCA in an attempt to validate its potential use as a functional in vivo marker. First, we quantified its relaxometric response in a complex 3D cell culture model. Subsequently, we examined potential changes in the functionality of primary glial cells following administration of this SCA. Monitoring intracellular Ca(2+) showed that, despite a reduction in the Ca(2+) level, transport of Ca(2+) through the plasma membrane remained unaffected, while stimulation with ATP induced Ca(2+)-transients suggested normal cellular signaling in the presence of low millimolar SCA concentrations. SCAs merely lowered the intracellular Ca(2+) level. Finally, we estimated the longitudinal relaxation times (T1) for an idealized in vivo fMRI experiment with SCA, for extracellular Ca(2+) concentration level changes expected during intense neuronal activity which takes place upon repetitive stimulation. The values we obtained indicate changes in T1 of around 1-6%, sufficient to be robustly detectable using modern MRI methods in high field scanners. Our results encourage further attempts to develop even more potent SCAs and appropriate fMRI protocols. This would result in novel methods that allow monitoring of essential physiological processes at the cellular and molecular level.
- [The protective effect of mild hypothermia pretreatment against injury to primary cultured cortical neurons induced of rat by glutamate]. [English Abstract, Journal Article]
- Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2014 Apr; 26(4):264-8.
To investigate the effect of mild hypothermia preconditioning against ischemia/reperfusion (I/R) injury of cultured primary cortical rats neurons, and to compare the protective effect of mild hypothermia only and with its combination with drugs.Cortical neurons of neonatal Sprague-Dawley (SD) rat within 24 hours after birth were harvested and cultured in vitro. On the 3rd day, the cells were cultured in a medium containing 2.5 mg/L cytosine arabinoside to inhibit the growth of glial cells and fibroblast. Having cultured for 6 days they were randomly divided into blank control group, glutamate damaged group (cultured with 200 μmol/L glutamate for 0.5 hour after washing), mild hypothermia preconditioning group (cultured under 33.5 centigrade for 24 hours before injury induced by glutamate), mild hypothermia combining with edaravone preconditioning group, and the hypothermia combining with propofol preconditioning group (medium containing 100 μmol/L edaravone and 3 mg/L propofol). They were cultured under 33.5 centigrade for 24 hours before injury induced by glutamate. After 24 hours of culturing in various medium, apoptosis ratio was observed by flow cytometry. Cell surviving rate was determined with methylthiazolete trazolium (MTT), c-fos protein expression was assayed, and morphologic change of cells with hematoxylin-eosin (HE) staining under the microscope, and ultrastructure changes were observed after uranyl acetate and lead citrate staining under transmission electron microscope.The apoptosis ratio and c-fos protein in glutamate damaged group were significantly higher than those in blank control group [apoptosis ratio: (9.85±0.76)% vs. (0.94±0.20)%, c-fos: 6.96±0.75 ng/L vs. 1.65±0.59 ng/L, both P<0.01], the cell surviving rate was significantly lower than that in blank control group [(0.20±0.02)% vs. (0.97±0.03)%, P<0.01]. Mild hypothermia preconditioning reversed surviving rate, apoptosis ratio and c-fos protein, and the effect of hypothermia combining with propofol preconditioning was obviously better [cell surviving rate: (0.80±0.04)% vs. (0.20±0.02)%, apoptosis ratio: (2.26±0.54)% vs. (9.85±0.76)%, c-fos: 2.98±0.46 ng/L vs. 6.96±0.75 ng/L, all P<0.01]. The morphology of cortical neurons in blank control group was normal. Most of the cells in glutamate damaged group showed bluish black cytoplasm with pyknic nuclei, with crimpled axons and of them were fractured, and cell number was obviously decreased. In each pre-conditional group, decrease in cell number was unconspicuous, and only a few cells showed apoptosis. Under transmission electron microscope, it was found that cell membrane, mitochondria and rough endoplasmic reticulum were intact in blank control group, but with reduction in organelles, severely swollen mitochondria, even with formation of vacuole or pyknosis, serious dilation of rough endoplasmic reticulum, with loss of cristac with loss of vacuoles or pyknosis, and marked dilatation of internal reticular endoplasm, and loss of cristac with vacuolation and chromatin were observed under electron microscope in glutamate damaged group. Compared with the glutamate damaged group, these pathologic changes were markedly alleviated in protected groups.Mild hypothermia preconditioning can inhibit glutamate-induced injury to cortical neurons. The protective effect of mild hypothermia combined with propofol is better.
- The Expansion of RPE Atrophy after the Inverted ILM Flap Technique for a Chronic Large Macular Hole. [Journal Article]
- Case Rep Ophthalmol 2014 Jan; 5(1):83-6.
To report a case of the expansion of submacular retinal pigment epithelium (RPE) atrophy after using the inverted internal limiting membrane (ILM) flap technique for a persisting, large, stage IV macular hole (MH).A 79-year-old woman presented with a chronic large MH that remained open despite pars plana vitrectomy (PPV). The surgery was performed twice for the MH closure 14 years earlier. ILM peeling was not performed during the previous surgeries. The best-corrected visual acuity (BCVA) with the Landolt ring chart was 0.08 at her visit. The minimum MH diameter was 1,240 μm. Inverted ILM flap technique with 20% SF6 gas tamponade was performed for the MH closure. For the inverted ILM flap technique, 25-gauge PPV and ILM staining with indocyanine green were used. The ILM was peeled off for 2 disc diameters around the MH, but the ILM was not removed completely. The ILM was then inverted and covered the MH.One month after surgery, the MH was closed, accompanied by glial cell proliferation spreading from the inverted ILM flap (as reported before). On the other hand, the area of the submacular RPE atrophy, which was already observed 1 week after surgery, gradually increased in size. BCVA improved to 0.3 six months after the surgery.The inverted ILM flap technique may be promising even for persisting large MH which were not closed in previous surgeries, but long-term observation is needed because the detailed behavior of the inverted ILM and the Müller cells after surgery is not yet known.
- Cellular Senescence Induced by Prolonged Subculture Adversely Affects Glutamate Uptake in C6 Lineage. [JOURNAL ARTICLE]
- Neurochem Res 2014 Apr 5.
Several researchers have recently used C6 cells to evaluate functional properties of high-affinity glutamate transporters. However, it has been demonstrated that this lineage suffers several morphological and biochemical alterations according to the number of passages in culture. Currently, there are no reports showing whether functional properties of high-affinity glutamate transporters comply with these sub culturing-dependent modifications. The present study aimed to compare the functional properties of high-affinity glutamate transporters expressed in early (EPC6) and late (LPC6) passage C6 cells through a detailed pharmacological and biochemical characterization. Between 60-180 min of L-[(3)H]glu incubation, LPC6 presented an intracellular [(3)H] 55 % lower than EPC6. Both cultures showed a time-dependent increase of intracellular [(3)H] reaching maximal levels at 120 min. Cultures incubated with D-[(3)H]asp showed a time-dependent increase of [(3)H] until 180 min. Moreover, LPC6 have a D-[(3)H]asp-derived intracellular [(3)H] 30-45 % lower than EPC6 until 120 min. Only EAAT3 was immunodetected in cultures and its total content was equal between them. PMA-stimulated EAAT3 trafficking to membrane increased 50 % of L-[(3)H]glu-derived intracellular [(3)H] in EPC6 and had no effect in LPC6. LPC6 displayed characteristics that resemble senescence, such as high β-Gal staining, cell enlargement and increase of large and regular nuclei. Our results demonstrated that LPC6 exhibited glutamate uptake impairment, which may have occurred due to its inability to mobilize EAAT3 to cell membrane. This profile might be related to senescent process observed in this culture. Our results suggest that LPC6 cells are an inappropriate glial cellular model to investigate the functional properties of high-affinity glutamate transporters.
- Cisplatin-induced alterations in the functional spermatogonial stem cell pool and niche in C57/BL/6J mice following a clinically relevant multi-cycle exposure. [JOURNAL ARTICLE]
- Toxicol Lett 2014 Apr 2.
A typical clinical cis-diamminedichloroplatinum(II) (cisplatin) dosing regimen consists of repeated treatment cycles followed by a recovery period. While effective, this dosing structure results in a prolonged, often permanent, infertility in men. Spermatogonial stem cells (SSCs) are theoretically capable of repopulating the seminiferous tubules after exposure has ceased. We propose that an altered spermatogonial environment during recovery from the initial treatment cycle drives an increase in SSC mitotic cell activity, rendering the SSC pool increasingly susceptible to cisplatin-induced injury from subsequent cycles. To test this hypothesis, the undifferentiated spermatogonia population and niche of the adult mouse (C57/BL/6J) were examined during the recovery periods of a clinically-relevant cisplatin exposure paradigm. Histological examination revealed a disorganization of spermatogenesis correlating with the number of exposure cycles. Quantification of terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick end labeling (TUNEL) staining indicated an increase in apoptotic frequency following exposure. Immunohistochemical examination of Foxo1 and incorporated BrdU showed an increase in the undifferentiated spermatogonial population and mitotic activity in the recovery period in mice exposed to one cycle, but not two cycles of cisplatin. Immunohistochemical investigation of glial cell line-derived neurotrophic factor (GDNF) revealed an increase in production along the basal Sertoli cell membrane throughout the recovery period in all treatment groups. Taken together, these data establish that the impact of cisplatin exposure on the functional stem cell pool and niche correlates with: (1) the number of dosing cycles; (2) mitotic activity of early germ cells; and (3) alterations in the basal Sertoli cell GDNF expression levels after cisplatin-induced testicular injury.
- Aquaporin-1 expression in proliferative vitreoretinopathy and in epiretinal membranes. [Journal Article]
- ScientificWorldJournal 2014.:876208.