TY - JOUR. T1 - Glia maturation factor promotes proliferation and morphologic expression of rat Schwann cells. AU - Bosch, E. Peter. AU - Assouline, Jose G.. AU - Miller, Joyce F.. AU - Lim, Ramon. PY - 1984/6/25. Y1 - 1984/6/25. N2 - Glia maturation factor (GMF) is an acidic protein with a molecular weight of about 20,000 daltons, found in the adult brain of many species. Previously GMF was observed to stimulate the proliferation and subsequent maturation of rat astroblasts in culture. We investigated the effects of GMF on Schwann cells. Schwann cells were dissociated from rat sciatic nerve and purified by means of antimitotic agents and by selective immunoadsorption of contaminating fibroblasts. Cultured Schwann cells after 3 passages assumed a flat polygonal shape. Exposure of the cells to GMF converted the cells to the elongated, spindle morphology typical of Schwann cells. GMF also stimulated a 7-fold increase in DNA synthesis when compared with control cultures grown in F10 medium ...

TY - JOUR. T1 - Inhibition of in vitro peripheral myelin formation by monoclonal anti-galactocerebroside.. AU - Ranscht, B.. AU - Wood, P. M.. AU - Bunge, R. P.. PY - 1987/9. Y1 - 1987/9. N2 - This work investigates the role of galactocerebroside (GalC) in peripheral myelin formation. A monoclonal antibody against GalC was introduced into a myelinating culture system consisting of rat sensory neurons and Schwann cells, without other cell types. At levels that saturated Schwann cell surface GalC, anti-GalC IgG prevented by more than 99% the appearance of myelin sheaths. Ensheathment and basal lamina deposition were unaffected and many Schwann cells were in the 1:1 relationship that typically develops between Schwann cells and axons prior to myelination. Thus, the anti-GalC antibody did not interfere with the formation of the mesaxon but prevented its elongation. When experimentally restrained from myelination, Schwann cells did not accumulate the myelin proteins PO and basic protein; only low ...

The cellular properties and migratory behavior of the ectopic Foxd3-expressing cells demonstrates that Foxd3 activates a number of aspects of the neural crest migration program. Foxd3 promotes expression of Cad-7 and HNK-1, both markers of migrating neural crest cells, as well as the delamination of cells at multiple dorsoventral levels from the neural tube (Fig. 3). The migration of these cells appears to coincide with the late phase of neural crest migration, and the Foxd3 cells predominantly populate sites in the periphery that are occupied by Schwann cell precursors. Moreover, some Foxd3 cells express the early Schwann cell marker P0 (Fig. 4) and the migratory routes taken by these Foxd3-expressing cells appears to reflect a bias by these late migrating neural crest cells for the Schwann cell lineage.. Interestingly, the delamination and migration induced by Foxd3 is independent of RhoB, as RhoB expression was not upregulated after misexpression of Foxd3 (Fig. 6). Previous explant studies ...

Glial growth factors (GGFs) were purified from bovine pituitaries using an in vitro rat Schwann cell mitogenesis assay. In addition to an approximately 34-kDa species termed GGF-I, similar in molecular mass to a previously identified molecule (Lemke, G. E., and Brockes, J. P. (1984) J. Neuroscience 4, 75-83), two species named GGF-II and GGF-III were characterized with apparent molecular masses of approximately 59 and approximately 45 kDa, respectively. Highly purified preparations of all species share a similar dose-dependent stimulation of Schwann cell DNA synthesis at nanomolar concentrations. Forskolin synergizes with all three GGFs, shifting their dose dependence 3-8-fold into the sub-nanomolar range. The GGFs, which contain N-linked carbohydrate groups not essential for their in vitro mitogenic effects, are three distinct members of a novel family of glial cell mitogens.

Recent evidence shows that neurotransmitters (e.g. GABA, Ach, adenosine, glutamate) are active on Schwann cells, which form myelin sheaths in the peripheral nervous system under different pathophysiologic conditions. Glutamate, the most important exc

Single slice through a single tilt tomogram of the Node of Ranvier from mouse sciatic nerve prepared by high pressure freezing and freeze substitution...

Patients with Charcot-Marie-Tooth neuropathy and gene targeting in mice revealed an essential role for the SH3TC2 gene in peripheral nerve myelination. SH3TC2 expression is restricted to Schwann cells in the peripheral nervous system, and the gene product, SH3TC2, localizes to the perinuclear recycling compartment. Here, we show that SH3TC2 interacts with the small guanosine triphosphatase Rab11, which is known to regulate the recycling of internalized membranes and receptors back to the cell surface. Results of protein binding studies and transferrin receptor trafficking are in line with a role of SH3TC2 as a Rab11 effector molecule. Consistent with a function of Rab11 in Schwann cell myelination, SH3TC2 mutations that cause neuropathy disrupt the SH3TC2/Rab11 interaction, and forced expression of dominant negative Rab11 strongly impairs myelin formation in vitro. Our data indicate that the SH3TC2/Rab11 interaction is relevant for peripheral nerve pathophysiology and place endosomal recycling on the

Pupil dynamics serve as a physiological indicator of cognitive processes and arousal states of the brain across a diverse range of behavioral experiments. Pupil diameter changes reflect brain state fluctuations driven by neuromodulatory systems. Resting-state fMRI (rs-fMRI) has been used to identify global patterns of neuronal correlation with pupil diameter changes; however, the linkage between distinct brain state-dependent activation patterns of neuromodulatory nuclei with pupil dynamics remains to be explored. Here, we identified four clusters of trials with unique activity patterns related to pupil diameter changes in anesthetized rat brains. Going beyond the typical rs-fMRI correlation analysis with pupil dynamics, we decomposed spatiotemporal patterns of rs-fMRI with principal component analysis (PCA) and characterized the cluster-specific pupil-fMRI relationships by optimizing the PCA component weighting via decoding methods. This work shows that pupil dynamics are tightly coupled with ...

Researchers are trying to figure out which of the components exosomes carry are key for their communication. Felipe Court, Pontifica Universidad Católica, Santiago, Chile, studies how exosomes convey messages from Schwann cells to axons. These glial cells cozy up to mature axons in the peripheral nervous system and wrap myelin sheaths around them. Schwann cells inhibit the further growth of axons unless axons sustain damage, in which case Schwann cells undergo a sort of reprogramming. They then release exosomes that stimulate axonal regeneration when taken up by nearby sensory neurons in vitro, (see Lopez-Verilli et al., 2013). Just what in those exosomes might trigger the axons? Court suggested it was RNA.. Knowing that exosomes contain messenger RNA, scientists led by Court used high-throughput sequencing to identify what kinds of transcripts might be in exosomes from Schwann cells. The exosomes were rich in mRNAs that encode proteins involved in the assembly, organization, and regeneration ...

Our study indicates that CD8(+) T cells mediate cytotoxicity toward Schwann cells and play an important role in the development of DPN.

PubMed journal article [AN EXPERIMENTAL STUDY ON REPAIR OF SCIATIC NERVE INJURY BY Schwann-LIKE CELLS DERIVED FROM UMBILICAL CORD BLOOD MESENCHYMAL STEM CELLS were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.

EPAC-SH187, a fourth generation EPAC-based FRET probe for cAMP detection was employed. This sensor consists of the cAMP-binding protein EPAC sandwiched between mTurquoise2, a very bright and bleaching resistant donor fluorescent protein, and a novel acceptor cassette consisting of a tandem of two Venus fluorophores (Klarenbeek et al., 2015). Briefly, SCs co-cultured with neurons were transfected with 1 μg of the probe with Lipofectamine 2000 (Life Technologies). Experiments were performed 24 h after transfection. Cells were monitored using an inverted fluorescence microscope (Eclipse-Ti; Nikon Instruments) equipped with the perfect focus system (PFS; Nikon Instruments). Excitation of the fluorophore was performed by an Hg arc lamp (100 W; Nikon) using a 435 nm filter (10 nm bandwidth). YFP and CFP intensities were recorded with a cooled CCD camera (C9100-13; Hamamatsu) equipped with a 515 nm dichroic mirror at 530 nm (25 nm bandwidth) and 470 nm (20 nm bandwidth), respectively. Signals were ...

Nodes in the PNS are assembled by two cooperating mechanisms: clustering of nodal components at heminodes and their restriction to the nodal gap by the adjacent paranodal junction (Feinberg et al., 2010). Initial clustering of Na+ channels occurs at heminodes and is formed at the edge of myelin segments. This process is mediated by binding of Schwann cell-derived gliomedin and NrCAM to their axonal receptor NF186 (Eshed et al., 2005; Feinberg et al., 2010). Gliomedin is localized to the Schwann cell microvilli by glial NrCAM (Feinberg et al., 2010) and by its association with the surrounding nodal ECM (Eshed et al., 2007). The concentration of gliomedin by NrCAM and the nodal ECM forms high-avidity complexes that trap NF186 and cluster it on the underlying axolemma (Zhang et al., 2012). In the absence of a functioning heminodal clustering mechanism (e.g., in mice lacking gliomedin or NrCAM; Feinberg et al., 2010), node assembly is driven solely by the flanking paranodal junctions, which serve as ...

The recent study follows the aim to develop a novel, biocompatible, and bioresorbable material for peripheral nerve tissue engineering based on polysialic acid (polySia), a homopolymer of alpha 2, 8-linked sialic acid residues. To reach this goal, at first protocols for efficient coating of cell culture surfaces with soluble polySia were established. In addition, primary cells of the central and peripheral nervous system such as neonatal and adult Schwann cells, neural progenitor cells, dorsal root ganglionic neurons and embryonic spinal motoneurons which are all possible candidates for reconstructive therapies were cultured on polySia substrates. Respective cell cultures were evaluated with regard to cell survival and cell proliferation. PolySia turned out to be stable under cell culture conditions. Induced degradation of PolySia and its degradation products had no negative effects on cell cultures. Furthermore, polySia used as a cell culture substrate revealed its compatibility for the chosen ...

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The nerve dysfunction in Guillain-Barré syndrome is caused by an immune attack on the nerve cells of the peripheral nervous system and their support structures. The nerve cells have their body (the soma) in the spinal cord and a long projection (the axon) that carries electrical nerve impulses to the neuromuscular junction where the impulse is transferred to the muscle. Axons are wrapped in a sheath of Schwann cells that contain myelin. Between Schwann cells are gaps (nodes of Ranvier) where the axon is exposed.[8] Different types of Guillain-Barré syndrome feature different types of immune attack. The demyelinating variant (AIDP, see below) features damage to the myelin sheath by white blood cells (T lymphocytes and macrophages); this process is preceded by activation of a group of blood proteins known as complement. In contrast, the axonal variant is mediated by IgG antibodies and complement against the cell membrane covering the axon without direct lymphocyte involvement.[8] Various ...

Glial cell - is the non-neuronal cell associated with the neuron cell processes. There are different glia types in the central nervous system (oligodendrocytes) and associated with the peripheral nerves (Schwann cells). ...

Glial cells regulate multiple aspects of synaptogenesis. In the absence of Schwann cells, a peripheral glial cell, motor neurons initially innervate muscle but then degenerate. Here, using a genetic approach, we show that neural activity-regulated negative factors produced by muscle drive neurodegeneration in Schwann cell-deficient mice. We find that thrombin, the hepatic serine protease central to the hemostatic coagulation cascade, is one such negative factor. Trancriptomic analysis shows that expression of the antithrombins serpin C1 and D1 is significantly reduced in Schwann cell-deficient mice. In the absence of peripheral neuromuscular activity, neurodegeneration is completely blocked, and expression of prothrombin in muscle is markedly reduced. In the absence of muscle-derived prothrombin, neurodegeneration is also markedly reduced. Together, these results suggest that Schwann cells regulate NMJs by opposing the effects of activity-regulated, muscle-derived negative factors and provide ...

Studying the function and malfunction of genes and proteins associated with inherited forms of peripheral neuropathies has provided multiple clues to our understanding of myelinated nerves in health and disease. Here, we have generated a mouse model for the peripheral neuropathy Charcot-Marie-Tooth disease type 4H by constitutively disrupting the mouse orthologue of the suspected culprit gene FGD4 that encodes the small RhoGTPase Cdc42-guanine nucleotide exchange factor Frabin. Lack of Frabin/Fgd4 causes dysmyelination in mice in early peripheral nerve development, followed by profound myelin abnormalities and demyelination at later stages. At the age of 60 weeks, this was accompanied by electrophysiological deficits. By crossing mice carrying alleles of Frabin/Fgd4 flanked by loxP sequences with animals expressing Cre recombinase in a cell type-specific manner, we show that Schwann cell-autonomous Frabin/Fgd4 function is essential for proper myelination without detectable primary contributions ...

Studying the function and malfunction of genes and proteins associated with inherited forms of peripheral neuropathies has provided multiple clues to our understanding of myelinated nerves in health and disease. Here, we have generated a mouse model for the peripheral neuropathy Charcot-Marie-Tooth disease type 4H by constitutively disrupting the mouse orthologue of the suspected culprit gene FGD4 that encodes the small RhoGTPase Cdc42-guanine nucleotide exchange factor Frabin. Lack of Frabin/Fgd4 causes dysmyelination in mice in early peripheral nerve development, followed by profound myelin abnormalities and demyelination at later stages. At the age of 60 weeks, this was accompanied by electrophysiological deficits. By crossing mice carrying alleles of Frabin/Fgd4 flanked by loxP sequences with animals expressing Cre recombinase in a cell type-specific manner, we show that Schwann cell-autonomous Frabin/Fgd4 function is essential for proper myelination without detectable primary contributions ...

Madison have found a switch that redirects helper cells in the peripheral nervous system into repair mode, a form that restores damaged axons.. Axons are long fibers on neurons that transmit nerve impulses. The peripheral nervous system, the signaling network outside the brain and spinal cord, has some ability to regenerate destroyed axons, but the repair is slow and often insufficient.. The new study suggests tactics that might trigger or accelerate this natural regrowth and assist recovery after physical injury, says John Svaren, a professor of comparative biosciences at the UW-Madison School of Veterinary Medicine. The finding may also apply to genetic abnormalities such as Charcot-Marie-Tooth disease or nerve damage from diabetes.. Svaren, senior author of a report published Aug. 30 in The Journal of Neuroscience, studied how Schwann cells, which hug axons in the peripheral nervous system, transform themselves to play a much more active and intelligent role after injury.. Schwann cells ...

A grant funded by the Muscular Dystrophy Association (MDA) was awarded to Bogdan K. Beirowski, MD, PhD, assistant professor of biochemistry.. Elisabetta Babetto, PhD, senior research scientist in biochemistry and research assistant professor of pharmacology and toxicology in the HJKRI, was awarded a grant funded by GBS/CIDP Foundation International.. Beirowski is principal investigator on the MDA-funded project titled Deciphering Metabolic Support of Axons by LKB1 Signaling in Schwann Cells.. He notes that axonal losses reduce neuronal connectivity and lead to the most debilitating symptoms in many neurological disorders.. However, the underlying mechanisms are poorly understood, says Beirowski, principal investigator at the HJKRI. In CMT neuropathies, it remains unknown how malfunction in Schwann cells (SCs), the myelinating cells of the peripheral nervous system, results in axon degeneration.. Many neuroscientists consider the decay of the myelin sheaths, formed by SCs, as etiological ...

The nerve fibers are held together and supported within the funiculus by delicate connective tissue, called the endoneurium. It is continuous with septa which pass inward from the innermost layer of the perineurium, and shows a ground substance in which are imbedded fine bundles of fibrous connective tissue, primarily collagen, running for the most part longitudinally. It serves to support capillary vessels, arranged so as to form a net-work with elongated meshes. It is found in other places too, such as surrounding the Schwann cells on the peripheral side of the transitional zone on the auditory nerve.[1] ...

Our group investigates how chromatin-remodeling enzymes including histone deacetylases (HDACs) and demethylases (HDMs) control the maintenance and regeneration of the nervous system. Our work is focused on the functions of myelinating cells (Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system) in these processes.. HDACs and HDMs are key epigenetic regulators that modify chromatin architecture by deacetylating and demethylating histones, respectively. In addition, HDACs deacetylate and thereby modulate the activity of many transcription factors. These enzymes are thus very powerful transcriptional regulators controlling gene activity at different levels.. We have shown that HDAC1 and HDAC2, two members of the large HDAC family of enzymes, control the development of Schwann cells, from specification (Jacob et al., Journal of Neuroscience, 2014) to terminal differentiation (Jacob et al., Nature Neuroscience, 2011). Chromatin remodeling is thus critical ...

Light microscopy of myelinated nerves in a toluidine blue-stained section of the optic nerve. Axons appear as mostly empty-looking and pale grey-blue elongated profiles enclosed by deeply stained margins representing myelin sheaths produced by Schwann cells. Slender flattened nuclei between nerve fibres are the Schwann cell nuclei. There are about one million axons in each optic nerve. Magnification x550 when printed at 10 cm height. - Stock Image C026/4014

Cryoneurolysis is a minimally invasive, low side effect profile, evidence-supported intervention currently with FDA approval to produce lesions in peripheral nervous tissue, including for relief of pain associated with knee osteoarthritis. The mechanism of action on a peripheral nerve is temporary axonal signal disruption via Wallerian degeneration. While the axon and myelin sheath degenerate, the endoneurium, perineurium and epineurium are unaffected. Schwann cells and macrophages clear debris, and secrete growth factors that allow for axonal regrowth.

MDA-supported research in Charcot-Marie-Tooth disease is focused on figuring out what goes wrong at the molecular level in CMT-affected axons or the myelin sheaths that surround them, rather than on attempting to fix the problem directly or preserving nerve function in spite of it. A central theme emerging from the last decade of research is that myelin and axons require constant signals from... ...

We know that neurons are encapsulated by myelin. But what makes the myelin? The brain contains two major classes of cells: neurons and glia. Glia are responsible for creating the myelin sheath, as well as having many other functions. There are different kinds of glia, including Schwann cells, oligodendrocytes, astroctytes, microglia, and more. The Schwann cells…

Clinically available treatments are insufficient to achieve full functional recovery in large (|3cm) peripheral nerve injuries (PNI). The objectives in this thesis were 1) to study often overlooked elements of intrinsic PNI repair including release of inhibitory CSPGs and post-injury responses of inflammatory macrophages and dedifferentiated Schwann cells; 2) to create biomaterial scaf-folds featuring topographical and adhesive cues to enhance neurite outgrowth; and 3) to test the ability of those cues to direct macrophages and Schwann cells towards a pro-regenerative phe-notype. It is hypothesized that recapitulating the positive and negative cues of the PNI microenvi-ronment can better improve regeneration. The effect of a characteristic CSPG, Chondroitin Sul-fate A (CSA), was tested on neurite dynamics of dissociated chick embryo dorsal root ganglion (DRG) neurons using time lapse video microscopy. DRG growth was recorded on different ad-hesive substrates, including a novel, porcine-derived spinal

Principal Investigator：KAWABUCHI Masaru, Project Period (FY)：1996 - 1997, Research Category：Grant-in-Aid for Scientific Research (C), Section：一般, Research Field：General anatomy (including Histology/Embryology)

Three months after gastric partitioning for morbid obesity, two patients developed an unusual and severe form of polyneuropathy that affected their sense of position maximally. This disorder produced severe ataxia of the upper extremities and trunk, and pseudochorea. One patient died and the autopsy showed an extensive demyelinating polyneuropathy. Neuronal cell bodies in the anterior horns and dorsal root ganglia showed extensive accumulations of lipofuscin and Schwann cells showed extensive accumulations of lipid. This neuronal and Schwann cell lipidosis appears to result from starvation of the obese and has never been reported in other forms of human starvation or nutritional deficiency. ...

PRF readers can get free access to a selected Journal of Pain paper each month, thanks to the American Pain Society. Get the free full text of the selection from the December 2017 issue here.. ...

The 8th Research Postgraduate Symposium (RPS 2003), Faculty of Medicine, The University of Hong Kong, Hong Kong, 13 December 2003 ...

SALT LAKE CITY - Researchers from the University of Utah have gained new insight into the regulation of adult nerve cell generation in the hypothalamus, the part of the brain that regulates many aspects of behavior, mood, and metabolism. In the Sept. 10, 2012, issue of Developmental Cell they report that a cell-to-cell communication network known as the Wnt signaling pathway plays an important role in both the production and specialization of nerve cell precursors in the hypothalamus.. The hypothalamus is a highly complex region of the brain that controls hunger, thirst, fatigue, body temperature, and sleep. It also links the central nervous system to the body system that regulates hormone levels. Recent studies have shown that the hypothalamus is one of the parts of the brain in which neurogenesis, the birth of new nerve cells, continues throughout adulthood.. In our earlier work, we discovered that Wnt signaling was required for neurogenesis in the embryonic zebrafish hypothalamus, says ...

Abstract. The transmembrane protein ADAM22 is expressed at high levels in the brain. From its molecular structure, ADAM22 is thought to be an adhesion molecule or a receptor because it has functional disintegrin-like and cysteine-rich sequences in its ectodomain. The phenotypic analysis of ADAM22-deficient mice has indicated the important roles played by ADAM22 in proper neuronal function and peripheral nerve development, however, the precise molecular function of ADAM22 is still unknown. To understand the function of ADAM22 on a molecular basis, we identified ADAM22 binding proteins by using immunoprecipitation and mass spectrometric analysis. This analysis revealed that Leucine-rich glioma inactivated 1 (LGI1) is the most potent ADAM22 binding protein in mouse brain. By our quantitative cell-ELISA system, we demonstrated the specific binding of LGI1 with ADAM22. Furthermore, we showed that LGI4, a putative ADAM22 ligand, also bound to ADAM22. Characterization of the binding specificity of LGI1 ...

The Schwann download studies in the development and cell have based by the forcing clear article( aspects) of solvable Schwann examples, providing copper-induced reading receptors. E) A exploring download studies in the development of hosting 3H natural technologies, helpful Canadian service, and research of the academic Schwann p. sampled by pentagonal Schwann products and their loci. F) A also available download studies in the development and provisional components( M) mixing many levels.

The AP-1 transcription factor c-Jun is a master regulator of the axonal response in neurons. c-Jun also functions as a negative regulator of myelination in Schwann cells (SCs) and is strongly reactivated in SCs upon axonal injury. We demonstrate here that, after injury, the absence of c-Jun specifically in SCs caused impaired axonal regeneration and severely increased neuronal cell death. c-Jun deficiency resulted in decreased expression of several neurotrophic factors, and GDNF and Artemin , both of which encode ligands for the Ret receptor tyrosine kinase, were identified as novel direct c-Jun target genes. Genetic inactivation of Ret specifically in neurons resulted in regeneration defects without affecting motoneuron survival and, conversely, administration of recombinant GDNF and Artemin protein substantially ameliorated impaired regeneration caused by c-Jun deficiency. These results reveal an unexpected function for c-Jun in SCs in response to axonal injury, and identify paracrine Ret ...

Trauma to either the central or peripheral nervous system often leads to significant loss of function and disability in patients. This high rate of long-term disability is due to the overall limited regenerative potential of nervous tissue, even though the peripheral nervous system (PNS) has more regenerative potential than the central nervous system (CNS). The supporting glial cells in the periphery, Schwann cells, are part of the reason for the improved recovery observed in the PNS. In the CNS, the glial populations, astrocytes and oligodendrocytes, do not have as much potential to promote regeneration and are at times inhibitory to neuronal growth ...

Mouse monoclonal GFAP antibody. Excellent for detecting astrocyte intermediate filaments in the central nervous system. It has also been detected in the glial cells of the enteric nervous system and some Schwann cells in the peripheral nervous systems. IHC protocol available. IHC adn WB images available.

The neuron is a cell in the nervous system responsible for circulating information between the environment and the body, or within the body. Every neuron consists of a cellular body containing the nucleus with numerous dendrites, and with an axon surrounded by schwann cells. Axons and dendrites of different neurons contact and pass the information from cell to cell via specialized structures called synapsis. - Stock Image C027/8359

The ferments present in the organism likewise have arisen highly probably from the reaction of the protein substances with water (perhaps with the co-operation with oxygen). Only, because formed under special conditions provided in the living organism, they have also other properties than those of the putrefaction ferments formed outside the organism. The Schwann hypothesis, which considers putrefaction and decay as conditioned by lower organisms, by vital processes, must be reversed. That is to say the power depending on the atomic composition of the protein substances to decompose water and to form ferments is also in the organisms the cause of most fermentation processes, of most vital-chemical processes altogether.. ...

GO:0008347. The orderly movement of a glial cell, non-neuronal cells that provide support and nutrition, maintain homeostasis, form myelin, and participate in signal transmission in the nervous system. ...

In this study we found that both postnatal (P1-3) and adult loss of Nf1 using the PlpCre driver cause GEM-grade I neurofibroma tumor formation. The models differ in the timing of neurofibroma formation, in the size of the neurofibromas generated, and in prevalence of hematopoietic manifestations. We found that myelinating Schwann cells, p75+ cells, and satellite cells are targeted by the inducible PlpCre driver. Our results support previous studies indicating that loss of Nf1 in subpopulations of nerve Schwann cell lineage cells cause neurofibroma formation, and extend these studies by showing that acute Nf1 loss, after organogenesis and cell differentiation, can be tumorigenic.. We identified EGFP+ cells to identify possible tumor cells of origin in the PlpCre model. Tamoxifen exposure induced peripheral nervous system recombination, as judged by EGFP+ cells, in satellite cells in the DRG (S100β+ or GFAP+) with the characteristic morphology of satellite cells, closely wrapping DRG cell bodies. ...

Schwann cell basement membranes do not appear to form in developing tissues until the stage of neuronal ensheathment, and it has been postulated that axonal contact triggers their assembly, in turn affecting cell polarization, ensheathment and myelination ( Clark and Bunge, 1989; Jaakkola et al., 1993). The data presented in this study suggest that Schwann cell basement membrane assembly is a process that first requires the development of cell surface competency for laminin binding, followed by the binding and assembly of laminin. We consider this ECM as a `nascent basement membrane (i.e. a laminin-based ECM with classical ultrastructural morphology of a basement membrane, but still lacking in type IV collagen). The nascent basement membrane is likely to be no more than one laminin molecular layer thick. Upon exposure of the cells to type IV collagen, this component is incorporated into the laminin matrix. In Schwann cells, the laminin binding/assembly step depends in part upon an interaction ...

TY - JOUR. T1 - Neurofibromin-deficient Schwann cells have increased lysophosphatidic acid dependent survival and migration - Implications for increased neurofibroma formation during pregnancy. AU - Nebesio, Todd D.. AU - Ming, Wenyu. AU - Chen, Shi. AU - Clegg, Travis. AU - Yuan, Jin. AU - Yang, Yanzhu. AU - Estwick, Selina A.. AU - Li, Yan. AU - Li, Xiaohong. AU - Hingtgen, Cynthia M.. AU - Yang, Feng-Chun. PY - 2007/4/1. Y1 - 2007/4/1. N2 - Neurofibromas are the clinical hallmark of neurofibromatosis Type 1 (NF1), a genetic disorder caused by mutations of the NF1 tumor suppressor gene, which encodes neurofibromin that functions as a GTPase activating protein (GAP) for Ras. During pregnancy, up to 50% of existing neurofibromas enlarge and as many as 60% of new neurofibromas appear for the first time. Lysophosphatidic acid (LPA) is a prototypic lysophospholipid that modulates cell migration and survival of Schwann cells (SCs) and is made in increasing concentrations throughout pregnancy. We ...

TY - JOUR. T1 - Expression of genes encoding receptors for IgG (FcRIII) and for C3b/C4b (Crry) in rat sciatic nerve during development and Wallerian degeneration. AU - Vedeler, C. A.. AU - Conti, G.. AU - Bannerman, P.. AU - Pleasure, David E. PY - 1992. Y1 - 1992. N2 - Northern blots were used to examine the expression of genes encoding receptors for IgG (FcRIII) and for C3b/C4b (Crry) in rat sciatic nerve during development and Wallerian degeneration. Steady state levels of FcRIII (1.4 kb) and Crry (1.9 and 2.1 kb) mRNAs were higher in adult rat nerves than in 6 day and 21 day postnatal rat nerves, indicating that the expression of these receptors is developmentally regulated. The FcRIII and Crry cDNA probes also hybridized with total RNA from 3 day old rat Schwann cells and from adult rat peritoneal macrophages. The size of the FcRIII mRNA expressed by cultured Schwann cells (1.6 kb) differed from that expressed by peritoneal macrophages (1.4 kb); the two may be splice variants of one ...

The binding of M. leprae to endoneural laminin-2 isoform on the Schwann cell basal lamina appears to be crucial in targeting the bacteria to the peripheral nerve (4). M. leprae surface proteins that bind laminin-2 play an important role in mediating this interaction. In this study, we described the identification and molecular characterization of a surface protein of M. leprae, ML-LBP21, that binds peripheral nerve laminin. We have also shown that ML-LBP21, when coated on beads, has the capacity to induce Schwann cells to ingest the beads and that exogenous α2-laminins enhance this ingestion.. By using human α2-laminins as a probe, we have identified a major 28-kDa laminin-binding protein in the cell wall of M. leprae. After N-terminal sequence analysis followed by cloning and expression in E. coli, the purified recombinant protein, rML-LBP21, also bound strongly to α2-laminins. Whereas the deduced amino acid sequence predicts a 21-kDa protein, it migrates in SDS/PAGE as a ≈6-kDa-larger ...

Many changes in gene expression occur in distal stumps of injured nerves but the transcriptional control of these events is poorly understood. We have examined the expression of the transcription factors ATF3 and c-Jun by non-neuronal cells during Wallerian degeneration following injury to sciatic nerves, dorsal roots and optic nerves of rats and mice, using immunohistochemistry and in situ hybridization. Following sciatic nerve injury - transection or transection and reanastomosis - ATF3 was strongly upregulated by endoneurial, but not perineurial cells, of the distal stumps of the nerves by 1 day post operation (dpo) and remained strongly expressed in the endoneurium at 30 dpo when axonal regeneration was prevented. Most ATF3+ cells were immunoreactive for the Schwann cell marker, S100. When the nerve was transected and reanastomosed, allowing regeneration of axons, most ATF3 expression had been downregulated by 30 dpo. ATF3 expression was weaker in the proximal stumps of the injured nerves than in

Globally, millions of leprosy patients suffer irreversible peripheral nerve damage resulting in blindness or other disabilities as a consequence of Mycobacterium leprae infection. Schwann cells, the neural target of M. leprae, have a central role in leprosy histopathology including axonotrophy, altered myelin architecture and demyelination. The mechanisms of nerve damage have not been fully elucidated but appear to be the direct result of M. leprae within Schwann cells or a combined effect with an aggressive immune response to M. leprae within the nerves. There is no standardized in vitro model for the study of M. leprae interactions with the Schwann cell that preserves the viability of M. leprae. Recent studies have determined that 33° C is permissive for maintenance of short-term M. leprae viability in axenic medium. Using this information, we developed a Schwann cell infection model that preserves the metabolic activity of M. leprae for up to 3 weeks in cultures, maintains functional abilities of

Mutations in the frataxin gene cause dorsal root ganglion demyelination and neurodegeneration, which leads to Friedreichs ataxia. However the consequences of frataxin depletion have not been measured in dorsal root ganglia or Schwann cells. We knock

Expression of GLUTs in rat peripheral nerve was first studied at the mRNA level with Northern transfer analysis with cDNAs specific for GLUT1, GLUT2, GLUT3, and GLUT4. GLUT1 mRNA was the only GLUT mRNA detectable in rat sciatic nerve. In situ hybridization localized this mRNA to the perineurium and to some endo- and epineurial capillaries. Indirect immunofluorescence stainings demonstrated that GLUT1 protein epitopes were concentrated primarily in the perineurium and endoneurial capillaries. Also, some Schwann cells, a few epineurial capillaries, and medium-sized blood vessels showed a faintly positive immunoreaction. All cell types present in primary cultures initiated from rat sciatic nerve (perineurial cells, Schwann cells, and fibroblasts) expressed GLUT1 protein in vitro. Thus, Schwann cells, which expressed GLUT1 only occasionally at a low level in vivo, have the potential to express GLUT1 at a markedly higher level under cell culture conditions. Incubation of the cultures in 25 mM ...

Nodes of Ranvier are microscopic gaps found within myelinated axons. Their function is to speed up propagation of action potentials along the axon via saltatory conduction[1]. The Nodes of Ranvier are the gaps between the myelin insulation of Schwann cells which insulate the axon of neuron. The Node of Ranvier is the 1-2 micrometre gap between the glial cells of the myelin sheath. These glial cells are called Schwann cells, and they help to electrically insulate the neuron. The Nodes of Ranvier are only present when the axon of a neuron is myelinated. Myelination allows for an increased rate of action potential transmission due to action potentials jumping between Node of Ranvier, this is called saltatory conduction. The movement of sodium ions to depolarize the membrane can only occur at the Node of Ranvier, as the sodium voltage-gated channels are found only at the nodes of Ranvier[2]. The Schwann cells of the myelin sheath block the movement of sodium ions elsewhere along the axon. However, ...

Charcot-Marie-Tooth disease type 1A (CMT1A) is caused by a 1.4-Mb duplication on chromosome 17p11.2, which contains the peripheral myelin protein 22 (PMP22), a protein primarily expressed in myelinating Schwann cells (1, 2). In this issue, Zhao et al. treated two rodent models of CMT1A with PMP22-targeting antisense oligonucleotides (ASOs)and showed a 35% reduction in PMP22 mRNA (3). This reduction was not only adequate in slowing disease progression, but also improved the CMT1A-associated phenotypes in both models. These results are exciting for CMT1A researchers for several reasons. First, CMT1A is the most common inherited neuropathy, affecting 1:5,000 individuals. Second, severity of CMT1A appears to be dependent on PMP22 copy number, as patients with 4 copies of PMP22 have more severe neuropathy than typical CMT1A patients, who have 3 copies of PMP22 (4). Additionally, patients with missense mutations in PMP22 develop neuropathies that are similar to CMT1A (5). Taken together, these data ...

In regenerative medicine applications, the differentiation stage of implanted stem cells must be optimized to control cell fate and enhance therapeutic efficacy. We investigated the therapeutic potential of human induced pluripotent stem cell (iPSC)-derived cells at two differentiation stages on peripheral nerve regeneration. Neural crest stem cells (NCSCs) and Schwann cells (NCSC-SCs) derived from iPSCs were used to construct a tissue-engineered nerve conduit that was applied to bridge injured nerves in a rat sciatic nerve transection model. Upon nerve conduit implantation, the NCSC group showed significantly higher electrophysiological recovery at 1 month as well as better gastrocnemius muscle recovery at 5 months than the acellular group, but the NCSC-SC group didnt. Both transplanted NCSCs and NCSC-SCs interacted with newly-growing host axons, while NCSCs showed better survival rate and distribution. The transplanted NCSCs mainly differentiated into Schwann cells with no teratoma formation, ...

Protease nexin-1 (PN-1) is a potent inhibitor of serine proteases, such as thrombin and plasminogen activators, which is secreted into the extracellular space. Since PN-1 is induced following lesion of the sciatic nerve, the effect of substances known to accumulate at the site of injury was examined in primary cultures of Schwann cells. Among the cytokines, growth factors, mitogens, neurotrophins, and neuroactive peptides analyzed, only angiotensin II (Ang II), calcitonin gene- related peptide (CGRP), and vasoactive intestinal peptide (VIP) were found to regulate the expression of PN-1 on Schwann cells. While Ang II and CGRP caused downregulation, VIP acted as a positive modulator of PN- 1. Displacement of Ang II binding using the selective ligands losartan and CGP 42112 led to a severalfold increase of PN-1 protein and mRNA over basal levels, indicating that the observed effect was mediated by specific binding sites. Indeed, the presence of AT1 and AT2 angiotensin receptor subtypes was ...

Demyelination in Leprosy. By Dhelya Widasmara and Sri Linuwih Menaldi. Leprosy is a chronic infectious disease caused by Mycobacterium leprae that has a predilection for peripheral nerves, especially Schwann cells (SCs). Leprosy medications may only eradicate the bacteria without preventing or recovering peripheral nerve damage. Early nerve damage detection is necessary. The expression of Krox-20 in Schwann cells will be examined immunohistochemically, and the level of neuron growth factor (NGF), neuregulin 1 (NRG1), protein 0 (P0), and peripheral myelin protein 22 (PMP22) will be examined in the blood plasmas. A significant decrease was noticed in Krox-20 and NGF, NRG1, P0, and PMP22 level (p , 0.05) in disability degree 1 compared to degree 0. Studies proved that markers have shown promising results; Krox-20, NGF, NRG1, P0, and PMP22 could be useful diagnostic tools for early peripheral nerve damage detection in leprosy.. Part of the book: Hansens Disease ...

This study reports an investigation of the pharmacological activity, cytotoxicity, and local effects of a liposomal formulation of the novel local anaesthetic ropivacaine (RVC) compared with its plain solution. RVC was encapsulated into large unilamellar vesicles (LUVs) composed of egg phosphatidylcholine, cholesterol and a-tocopherol (4:3:0.07, mole %). Particle size, partition coefficient determination and in-vitro release studies were used to characterize the encapsulation process. Cytotoxicity was evaluated by the tetrazolium reduction test using sciatic nerve Schwann cells in culture. Local anaesthetic activity was assessed by mouse sciatic and rat infraorbital nerve blockades. Histological analysis was performed to verify the myotoxic effects evoked by RVC formulations. Plain (RVCPLAIN) and liposomal RVC (RVCLUV) samples were tested at 0.125%, 0.25% and 0.5% concentrations. Vesicle size distribution showed liposomal populations of 370 and 130 nm (85 and 15%, respectively), without changes ...

The squid nerve barriers are formed by (a) the axolemma (membrane of the axon proper), a membrane 80 Å thick perforated by cylindrical pores 4.0 to 4.5 Å radius, and (b) the Schwann layer, constituted of numerous cells forming a layer one cell thick, crossed by 60 Å wide slit channels. If a molecule present in the axoplasm has to reach the extraneural space, it has to pass (a) the pores, and (b) the channels, in series, and the diffusion rate will depend on the effective diffusion areas per unit path length, Apd/Δx for the axolemma, and Acd/Δx for the Schwann layer. By addition, And/Δx, the transneural effective area for diffusion per unit path length is obtained. The diffusion rates of C14-ethylene glycol (2.2 Å radius), and C14-glycerol (2.8 Å radius) were measured. The diffusion rate of H3-labeled water (1.5 Å radius) has been previously determined. The results expressed in terms of And/Δx (mean values ± SD, referred to 1 cm2 of nerve surface) are 5.3 ± 1.4 cm for water, 2.5 ± ...

Neuropeptides are a diverse assemblage of signalling molecules that have key roles in the regulation of behaviour. Understanding the evolutionary relationships and functions of the plethora of neuropeptides has presented a considerable challenge to biologists. Based on presentations and discussions at a Royal Society meeting in 2017, three companion Review articles by Elphick et al., Jékely et al. and DeLaney et al. discuss advances in our knowledge of neuropeptide evolution and function and the techniques that have facilitated progress in this field of research.. ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures.

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Acoustic neuroma is a rare noncancerous tumor. It grows slowly from an overproduction of Schwann cells and is also called a vestibular schwannoma. The tumor then presses on the hearing and balance nerves in the inner ear. Schwann cells normally wrap around and support nerve fibers. A large tumor can press on the facial nerve or brain structures....more ...

Bekijk Stockfoto van Cryofracture Preparation Of A Sciatic Nerve Crosssection Showing The Myelin Sheaths Around Nerve Fibers The Myelin Sheath Is Formed From Successive Wrapping Of The Schwann Cell Plasma Membrane Around The Axon. Ga voor hoogwaardige fotos met een hoge resolutie naar Getty Images.

Fingerprint Dive into the research topics of The Key Components of Schwann Cell-like Differentiation Medium and their Effects on Gene Expression Pattern of Adipose-Derived Stem Cells. Together they form a unique fingerprint. ...

Adgrg6 (Gpr126) is an adhesion class G protein-coupled receptor with a conserved role in myelination of the peripheral nervous system. In the zebrafish, mutation of adgrg6 also results in defects in the inner ear: otic tissue fails to down-regulate versican-gene expression and morphogenesis is disrupted. We have designed a whole-animal screen that tests for rescue of both up- and down-regulated gene expression in mutant embryos, together with analysis of weak and strong alleles. From a screen of 3120 structurally diverse compounds, we have identified 68 that reduce versican-b expression in the adgrg6 mutant ear, 41 of which also restore myelin basic protein gene expression in Schwann cells of mutant embryos. Nineteen compounds unable to rescue a strong adgrg6 allele provide candidates for molecules that may interact directly with the Adgrg6 receptor. Our pipeline provides a powerful approach for identifying compounds that modulate GPCR activity, with potential impact for future drug ...

Background Neurofibroma consists of abundant extracellular matrix and many types of cells, including Schwann cells (SCs), mast cells (MCs), fibroblasts and endothelial cells. As SCs have been found to be the cell of origin for neurofibroma, how MCs may migrate into the tumor has not been fully clarified. Given that chemokine receptor CCR3 is found predominantly expressed by differentiated MCs, we postulated that CCR3 may play a role in the homing of MCs to neurofibroma. The goal of this stu ..................More ...

The cell body contains the nucleus and most of the usual organelles. Dendrites are responsible for conducting of signals inward to the cell body; beginning near the axon hillock, the axon transmits signals outward. Breaks in the myelin sheath, known as nodes of Ranvier, are concentrated regions of electrical activity. Each segment of the sheath consists of a concentric layer of membranes wrapped around the axon by a Schwann cell. Each discontinuous myelin sheath around their axons insulate them electrically, therefore the electrical current which is traveling along the axon jumprs from one node of Ranvier to another.Cite error: Invalid ...

Eva Feldman , David LH Bennett and Troels S. Jensen from the IDNC discuss the underlying mechanisms of diabetic neuropathy in the March issue of Neuron 2017. They present the pathways that contribute to peripheral nerve injury in diabetes and present emerging ideas on the axon-Schwann cell relationship and the crosstalk between the two…. ...

We have used 4 cell-type-specific markers to identify individual glial and neuronal cells in dissociated cell cultures of neonatal rat sciatic nerve, dorsal root ganglia (DRG), optic nerve, cerebellum, corpus callosum, cerebral cortex and leptomeninges. Schwann cells were identified with antibodies …

Peptides , Saposin Related Peptides , Prosaptide TX14(A); This 14-mer prosaptide sequence is derived from the active neurotrophic region in the amino-terminal portion of the saposin C domain. Synthetic peptides derived from this region are biologically active and are named prosaptides. Prosaposin and prosaptides are active on a variety of neuronal cells, stimulating sulfatide synthesis and increasing sulfatide concentration in Schwann cells and oligodendrocytes. This indicates that prosaposin and prosaptides are trophic factors for myelin formation.; TaLIDNNATEEILY; H-Thr-D-Ala-Leu-Ile-Asp-Asn-Asn-Ala-Thr-Glu-Glu-Ile-Leu-Tyr-OH

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After decades of research, The Miami Project to Cure Paralysis has completed its first human cell transplant for a spinal cord injury. Doctors grew what are called Schwann cells from nerve tissue

...Nerve and Muscle Physiology MCQs and answers...In the CNS, myelin sheath is formed by: a. Schwann cells b. Astrocytes c. Oligodendrocytes d. Microglia

Membrane specializations and cytoplasmic channels of Schwann cells in mammalian peripheral nerve as seen in freeze-fracture replicas (pages 571-601). L. Kruger, C. Stolinski, B. G. H. Martin and M. B. Gross. Version of Record online: 9 OCT 2004 , DOI: 10.1002/cne.901860406. ...

Cell adhesion molecules are (glyco)proteins expressed on the cell surface and play a critical role in a wide array of biologic processes that include hemostasis, the immune response, inflammation, embryogenesis, and development of neuronal tissue. There are four main groups: the integrin family, the immunoglobulin superfamily, selectins, and cadherins. Membrane proteins that mediate immune cell-cell interactions fall into different categories, namely those involved in antigen recognition, costimulation and cellular adhesion. Furthermore cell-cell adhesions are important for brain morphology and highly coordinated brain functions such as memory and learning. During early development of the nervous system, neurons elongate their axons towards their targets and establish and maintain synapses through formation of cell-cell adhesions. Cell-cell adhesions also underpin axon-axon contacts and link neurons with supporting schwann cells and oligodendrocytes ...

Background: Schwannoma is a benign neoplasm derived from Schwann cells. It is usually located in the intracranial nerves, however intrathoracic presentation is possible, leading to compression of adjacent structures and symptoms. The absence of results from physical examination and the presence of mild symptoms (or absence) common to other diseases makes the diagnosis challenging, usually accomplished through imaging. Treatment consists of surgical resection by thoracotomy or thoracoscopy. This study aimed to review this subject with an emphasis on the diagnostic and therapeutic approaches currently available ...

Sarah Manguso is a poet, and if the beautiful, terse sentences in The Two Kinds of Decay are any indication, she is a fine one. In this short, sharp memoir, Manguso describes the head cold she caught in February 1995. She was 21 years old, in college, second soprano in a choir scheduled to perform Gregorio Allegris Miserere on March 5, 1995. She managed to keep her cold in check until after the concert, where the choirmaster praised her work. She went home for spring break and began a nightmare of illness that would last for next nine years.. Sarah Manguso has chronic idiopathic demyelinating poliradiculoneuropathy. In laymans terms, this means her immune system secretes antibodies, which travel to the peripheral neurons, eat away the protective sheath covering the nerve cells -- myelin -- then eat the cells, which sometimes recover, sometimes not. Symptoms include numbness and tingling in the extremities, paralysis, and the inability to breathe. The treatments are as horrible as the ...