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glial cell membrane [keywords]
- A spinal tumor showing mixed features of ependymoma and hemangioblastoma: a case report and literature review. [JOURNAL ARTICLE]
- Brain Tumor Pathol 2014 Dec 17.
We report an intramedullary spinal tumor consisting of an ependymoma and a hemangioblastoma (HB). A 37-year-old woman presented with progressive bilateral lower limb sensory and motor deficits. Magnetic resonance imaging showed a single intramedullary mass in the thoracic cord (T4-T6 level). Clinically, the patient had no von Hippel-Lindau disease and neurofibromatosis type 2. Metastatic carcinomas including renal cell carcinoma were altogether negative. Complete surgical resection was performed. Histologically, the tumor consisted of a mixed ependymoma and HB. Tumor cells of ependymoma displayed a rather uniform appearance with round to oval nuclei having salt-and-pepper-like chromatin, forming perivascular pseudorosette structures with radially arranged, tapering cell processes extending to intratumoral blood vessels. Stromal cells of HB had vacuolated or homogeneously eosinophilic cytoplasm and variable sized hyperchromatic nuclei within a background of capillaries. Immunohistochemically, tumor cells of ependymoma were strongly positive for glial fibrillary acidic protein (GFAP), focally positive for epithelial membrane antigen (EMA) and D2-40 in a dot-like or ring-like pattern. Stromal cells of HB showed immunoreactivity for S100, vimentin, inhibin-α, D2-40, EMA and cytokeratins (CK: AE1/AE3, CK19). A review of the literature, in conjunction with the present case, shows that ependymomas and HBs may have a close relationship with each other.
- Premyelinated central axons express neurotoxic NMDA receptors: relevance to early developing white-matter injury. [JOURNAL ARTICLE]
- J Cereb Blood Flow Metab 2014 Dec 17.
Ischemic-type injury to developing white matter is associated with the significant clinical condition cerebral palsy and with the cognitive deficits associated with premature birth. Premyelinated axons are the major cellular component of fetal white matter and loss of axon function underlies the disability, but the cellular mechanisms producing ischemic injury to premyelinated axons have not previously been described. Injury was found to require longer periods of modelled ischemia than at latter developmental points. Ischemia produced initial hyperexcitability in axons followed by loss of function after Na(+) and Ca(2+) influx. N-methyl-D-aspartate- (NMDA) type glutamate receptor (GluR) agonists potentiated axon injury while antagonists were protective. The NMDA GluR obligatory Nr1 subunit colocalized with markers of small premyelinated axons and expression was found at focal regions of axon injury. Ischemic injury of glial cells present in early developing white matter was NMDA GluR independent. Axons in human postconception week 18 to 23 white matter had a uniform prediameter expansion phenotype and postembedded immuno-gold labelling showed Nr1 subunit expression on the membrane of these axons, demonstrating a shared key neuropathologic feature with the rodent model. Premyelinated central axons therefore express high levels of functional NMDA GluRs that confer sensitivity to ischemic injury.Journal of Cerebral Blood Flow & Metabolism advance online publication, 17 December 2014; doi:10.1038/jcbfm.2014.227.
- A comparative study of LAMPs and YKL-40 tissue expression in glial tumors. [Journal Article, Research Support, Non-U.S. Gov't]
- Folia Med (Plovdiv) 2014 Jul-Sep; 56(3):194-8.
YKL-40 is a glycoprotein believed potentially to be a marker of various pathological processes. High levels of YKL-40 have been found in cancer and chronic inflammatory diseases. The function of the glycoprotein is not completely known yet. A possible involvement in angiogenesis and tumor aggressiveness is supposed. Lysosome-associated membrane glycoproteins (LAMP) 1 and 2 are highly conserved proteins with still undefined biological functions. There is evidence that they are implicated in autophagy, angiogenesis and tissue remodeling.The aim of the present study was to investigate the potential relationship between the tissue expression of YKL-40, LAMP-1 and LAMP-2 in glial tumors.LAMPs and YKL-40 expression was determined by immunohistochemistry in 36 glial tumors. A morphometric analysis of the intensity of tissue expression was performed with the Quick-photo Micro 2.3. system. Area (μm), perimeter (μm), and expression level (%) of the three glycoproteins were calculated.LAMPs were found on cell membranes of glial and endothelial cells, while YKL-40 was detected in the cytoplasm of these cells. Intensive immunohistochemical reaction was present in tumor cells. LAMP-2 showed a more intensive staining compared to LAMP-1.We present the first comparative study of YKL-40 and LAMPs in astroglial tumors. The relationship between the expression of the three glycoconjugates indicates a possible participation in the processes of angiogenesis and tissue remodeling during tumor development.
- Sensing deep extreme environments: the receptor cell types, brain centers, and multi-layer neural packaging of hydrothermal vent endemic worms. [Journal Article]
- Front Zool 2014; 11(1):82.
Deep-sea alvinellid worm species endemic to hydrothermal vents, such as Alvinella and Paralvinella, are considered to be among the most thermotolerant animals known with their adaptability to toxic heavy metals, and tolerance of highly reductive and oxidative stressful environments. Despite the number of recent studies focused on their overall transcriptomic, proteomic, and metabolic stabilities, little is known regarding their sensory receptor cells and electrically active neuro-processing centers, and how these can tolerate and function in such harsh conditions.We examined the extra- and intracellular organizations of the epidermal ciliated sensory cells and their higher centers in the central nervous system through immunocytochemical, ultrastructural, and neurotracing analyses. We observed that these cells were rich in mitochondria and possessed many electron-dense granules, and identified specialized glial cells and serial myelin-like repeats in the head sensory systems of Paralvinella hessleri. Additionally, we identified the major epidermal sensory pathways, in which a pair of distinct mushroom bodies-like or small interneuron clusters was observed. These sensory learning and memory systems are commonly found in insects and annelids, but the alvinellid inputs are unlikely derived from the sensory ciliary cells of the dorsal head regions.Our evidence provides insight into the cellular and system-wide adaptive structure used to sense, process, and combat the deep-sea hydrothermal vent environment. The alvinellid sensory cells exhibit characteristics of annelid ciliary types, and among the most unique features were the head sensory inputs and structure of the neural cell bodies of the brain, which were surrounded by multiple membranes. We speculated that such enhanced protection is required for the production of normal electrical signals, and to avoid the breakdown of the membrane surrounding metabolically fragile neurons from oxidative stress. Such pivotal acquisition is not broadly found in the all body parts, suggesting the head sensory inputs are specific, and these heterogenetic protection mechanisms may be present in alvinellid worms.
- Relationship between rat retinal degeneration and potassium channel KCNQ5 expression. [JOURNAL ARTICLE]
- Exp Eye Res 2014 Dec 10.:1-11.
KCNQ5/Kv7.5 is a low-threshold non-inactivating voltage-gated potassium channel preferentially targeted to excitatory endings in brain neurons. The M-type current is mediated by KCNQ5 channel subunits in monkey retinal pigment epithelium cells and in brain neurons. This study was undertaken to analyze KCNQ5 expression and the interaction signals of KCNQ5 with other proteins in normal rat retina and during photoreceptor degeneration. The KCNQ5 expression pattern was studied by immunocytochemistry and Western blot in normal rat retinas (Sprague-Dawley, SD) and P23H-1 rats as a retinitis pigmentosa model. The physical interactions of KCNQ5 with calmodulin (CaM), vesicular glutamate transporter 1 (VGluT1) and glial fibrillary acidic protein (GFAP) were analyzed by in situ proximity ligation assays and were supported by calcium recording. KCNQ5 expression was found in the plexiform layers, ganglion cell layer and basal membrane of the retinal pigment epithelium. The physical interactions among KCNQ5 and CaM, VGluT1 and GFAP changed with age and during retinal degeneration. The maximal level of KCNQ5/CaM interaction was found when photoreceptors had almost completely disappeared; the KCNQ5/VGluT1 interaction signal decreased and the KCNQ5/GFAP interaction increased in the inner retina, while degeneration progressed. The basal calcium levels in the astrocytes and neurons of P23H-1 were higher than in the control SD retinas. This study demonstrates that KCNQ5 is present in the rat retina where its activity may be moderated by CaM. Retinal degeneration progression in P23H-1 rats can be followed by an interaction between KCNQ5 with CaM in an in situ system. The relationship between KCNQ5 and VGluT1 or GFAP needs to be more cautiously interpreted.
- Effect of prenatal exposure to LPS combined with pre- and post-natal high-fat diet on hippocampus in rat offspring. [JOURNAL ARTICLE]
- Neuroscience 2014 Dec 10.
Prenatal exposure to lipopolysaccharide (LPS) or high-fat diet (HFD) results in hippocampal impairment and cognitive deficits in offspring rats. What is not clear is how prenatal exposure to LPS combined with pre- and post-natal HFD would affect the hippocampus in offspring rats.32 pregnant rats were randomly divided into four groups, including control group; LPS group (pregnant rats were injected with LPS 0.4mg/kg intraperitoneally on the 8th, 10th and 12th day of pregnancy); HFD group (maternal rats had HFD during pregnancy and the lactation period, and their pups also had HFD up to the third month of life); LPS+HFD group (rats were exposed to the identical experimental scheme with LPS group and HFD group). The serum IL-6 and TNF-alpha concentration was measured in three-month-old offspring rats in all groups. Hippocampal morphology and expressions of glial fibrillary acidic protein (GFAP), Tau and synaptophysin (SYP) in offspring rats were measured.Serum IL-6 and TNF-alpha concentration in the HFD group increased significantly compared with the control group, LPS group and LPS+HFD group. Compared with the control group and the LPS+HFD group, cells in the LPS and HFD groups were smaller and arranged in disorder, and cell membrane was not complete, nucleoli and nuclear heterochromatin stained darkly with hematoxylin. GFAP and Tau expression in the hippocampus of the LPS and HFD groups increased significantly compared with the control group and LPS+HFD group. SYP expression in the LPS and HFD groups decreased significantly compared with the control group and HFD group, increased in the LPS+HFD group.Prenatal exposure to LPS combined with pre- and post-natal HFD result in a protective effect on the hippocampus in offspring rats, and it might be a benefit from the predictive adaptive response to prenatal inflammation.
- Fetal presentation of congenital fibrosarcoma of the meninges: case report and literature review. [JOURNAL ARTICLE]
- Clin Neuropathol 2014 Dec 5.
Aim:Congenital infantile fibrosarcoma (CIFS) exceptionally occurs in the meninges, with no cases reported beforeor at birth. We report herein a meningeal CIFS diagnosed in a fetus at 40 weeks of gestation (WG). Case report: A 24-yearoldpregnant woman was referred to theobstetricsdepartment for vaginal bleeding. A severe right hydrocephalus due to a large tumor invading the left hemisphere and ventricles was discovered in the fetus, and medical termination of the pregnancy was achieved.
Results:Histological examination revealed a highly cellular spindle or ovoid shaped cell proliferation organized in interlacing bundles; it was diffusely positive for vimentin, and scarcely for SMA (smooth muscle actin). NFs (neurofilaments), NeuN, S100 protein, desmin, GFAP (glial fibrillary acidic protein), Olig2, chromogranin, synaptophysin, CD31, CD34, BCL2, and EMA (epithelial membrane antigen) antibodies were negative. Ki67 antibody labeled 20% of the nuclei. A reverse transcription polymerase chain reaction assay was performed to detect the gene fusion ETV6-NTRK3 transcript. Despite negative results, it was concluded to be a CIFS of the meninges. Discussion: CIFS of the meninges during the fetal period has never been reported. Its diagnosis is based on immunohistochemistry, and, whenever possible, on the detection of the reciprocal translocation t (12;15) resulting in the gene fusion ETV6-NTRK3. Its prognosis depends on rapid growth and local invasiveness leading to cerebral structure damage.
- CNS Myelination Requires Cytoplasmic Dynein Function. [JOURNAL ARTICLE]
- Dev Dyn 2014 Dec 8.
Background:Cytoplasmic dynein provides the main motor force for minus-end-directed transport of cargo on microtubules. Within the vertebrate central nervous system (CNS), proliferation, neuronal migration and retrograde axon transport are among the cellular functions known to require dynein. Accordingly, mutations of DYNC1H1, which encodes the heavy chain subunit of cytoplasmic dynein, have been linked to developmental brain malformations and axonal pathologies. Oligodendrocytes, the myelinating glial cell type of the CNS, migrate from their origins to their target axons and subsequently extend multiple long processes that ensheath axons with specialized insulating membrane. These processes are filled with microtubules, which facilitate molecular transport of myelin components. However, whether oligodendrocytes require cytoplasmic dynein to ensheath axons with myelin is not known.
Results:We identified a mutation of zebrafish dync1h1 in a forward genetic screen that caused a deficit of oligodendrocytes. Using in vivo imaging and gene expression analyses, we additionally found evidence that dync1h1 promotes axon ensheathment and myelin gene expression.
Conclusions:In addition to its well known roles in axon transport and neuronal migration, cytoplasmic dynein contributes to neural development by promoting myelination. This article is protected by copyright. All rights reserved.
- Matrix metalloproteinase-14 both sheds cell surface NG2 proteoglycan on macrophages and governs the response to peripheral nerve injury. [JOURNAL ARTICLE]
- J Biol Chem 2014 Dec 8.
Neuronal glial antigen 2 (NG2) is an integral membrane chondroitin sulfate proteoglycan, expressed by vascular pericytes, macrophages (NG2-Mϕ) and progenitor glia of the nervous system. Herein, we revealed that NG2 shedding and axonal growth, either independently or jointly, depended on the pericellular remodeling events executed by membrane-type 1 matrix metalloproteinase (MT1-MMP/MMP-14). Using purified NG2 ectodomain constructs, individual MMPs and primary NG2-Mϕ cultures, we demonstrated, for the first time, that MMP-14 performed as an efficient and unconventional NG2 sheddase, and that NG2-Mϕ infiltrated into the damaged PNS. We then characterized the spatio-temporal relationships among MMP-14, MMP-2, and TIMP-2 (tissue inhibitor of metalloproteinases-2) in sciatic nerve. TIMP-2-free MMP-14 was observed in the primary Schwann cell cultures using the inhibitory hydroxamate warhead-based MP-3653 fluorescent reporter. In teased nerve fibers, MMP-14 translocated post-injury towards the nodes of Ranvier and its substrates, laminin and NG2. Inhibition of MMP-14 activity, using the selective, function-blocking DX2400 human monoclonal antibody, increased the levels of regeneration-associated factors, including laminin, GAP-43 and ATF3, thereby promoting sensory axon regeneration after nerve crush. Concomitantly, DX2400 therapy attenuated mechanical hypersensitivity associated with nerve crush in rats. Together, our findings describe a new model in which MMP-14 proteolysis regulates the extracellular milieu and presents a novel therapeutic target in the damaged PNS and neuropathic pain.
- Activation of α7 nicotinic acetylcholine receptors protects astrocytes against oxidative stress-induced apoptosis: Implications for Parkinson's disease. [JOURNAL ARTICLE]
- Neuropharmacology 2014 Dec 5.
Astrocytes have been implicated in the immune responses associated with Parkinson's disease (PD). Inhibition of astrocyte apoptosis is a novel strategy for the treatment of PD. Recent studies suggest that α7 nicotinic acetylcholine receptors (α7-nAChRs) expressed in glial cells are critical links between inflammation and neurodegeneration in PD. However, little is known about their contribution to astrocyte apoptosis during the development of this disorder. In the present study, we showed that nicotine exerts a protective effect on H2O2-induced astrocyte apoptosis and glial cell-derived neurotrophic factor (GDNF) downregulation, and this effect was abolished by an α7-nAChR-selective antagonist. The underlying mechanisms might involve alleviation of mitochondrial membrane potential loss, stabilization of the Bax/Bcl-2 balance, and inhibition of cleaved caspase-9 activity through α7-nAChR activation. Systemic administration of nicotine dramatically alleviated MPTP-induced symptoms, protected dopaminergic neurons against degeneration, inhibited astrocytes and microglia activation in the substantia nigra pars compacta (SNpc) and blocked the decrease of GDNF in the striatum by activating α7-nAChRs. Taken together these findings demonstrate, for the first time, that nicotine suppresses H2O2-induced astrocyte apoptosis via the mitochondrial pathway through the stimulation of α7-nAChRs. Targeting α7-nAChRs expressed in astrocytes may be a novel therapeutic strategy for the treatment of neurodegenerative disorders.