scholarly journals Fibronectin promotes rat Schwann cell growth and motility.

1982 ◽  
Vol 93 (1) ◽  
pp. 211-216 ◽  
Author(s):  
A Baron-Van Evercooren ◽  
H K Kleinman ◽  
H E Seppä ◽  
B Rentier ◽  
M Dubois-Dalcq
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Tritiated Thymidine ◽  
Primary Cultures ◽  
Boyden Chamber ◽  
Low Concentrations ◽  
And Migration ◽  
Thymidine Autoradiography ◽  
Double Immunolabeling

Techniques are now available for culturing well characterized and purified Schwann cells. Therefore, we investigated the role of fibronectin in the adhesion, growth, and migration of cultured rat Schwann cells. Double-immunolabeling shows that, in primary cultures of rat sciatic nerve, Schwann cells (90%) rarely express fibronectin, whereas fibroblasts (10%) exhibit a granular cytoplasmic and fibrillar surface-associated fibronectin. Secondary cultures of purified Schwann cells do not express fibronectin. Exogenous fibronectin has a small effect on promoting the adhesion of Schwann cells to the substrate and does not significantly affect cell morphology, but it produced a surface fibrillar network on fibronectin on the secondary Schwann cells. Tritiated thymidine autoradiography revealed that addition of fibronectin to the medium, even at low concentrations, markedly stimulates Schwann cell proliferation, in both primary and secondary cultures. In addition, when cell migration was measured in a Boyden chamber assay, fibronectin was found to moderately, but clearly, stimulate directed migration or chemotaxis.

scholarly journals Octopaminergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre

1986 ◽  
Vol 121 (1) ◽  
pp. 421-443 ◽  
Author(s):  
V. Reale ◽  
P. D. Evans ◽  
J. Villegas
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Nerve Fibre ◽  
High Frequency ◽  
Cell Activity ◽  
Physiological Role ◽  
Giant Axon ◽  
Octopamine Receptors ◽  
Low Concentrations

The actions of octopamine on the Schwann cells of the giant nerve fibre of the tropical squid are described. The pharmacology of the receptors mediating the actions of octopamine has been investigated in terms of stereospecificity, amine specificity and interactions with a range of agonists and antagonists. The receptors are maximally activated by D(−)-octopamine and share many of the characteristics of OCTOPAMINE2 class receptors in other preparations. The octopamine receptors appear to mediate their actions by increasing the intracellular levels of cyclic AMP in the Schwann cells. Low concentrations of octopamine potentiate the actions of the nicotinic cholinergic activation system of the Schwann cells. The results are discussed in terms of the possible physiological role of octopamine in the modulation of Schwann cell activity during stressful conditions when the giant axon system is likely to be used at a high frequency to facilitate the escape response of the squid.

scholarly journals Interleukin-4 Regulates the Expression of CD209 and Subsequent Uptake of Mycobacterium leprae by Schwann Cells in Human Leprosy

2010 ◽  
Vol 78 (11) ◽  
pp. 4634-4643 ◽  
Author(s):  
Rosane M. B. Teles ◽  
Stephan R. Krutzik ◽  
Maria T. Ochoa ◽  
Rosane B. Oliveira ◽  
Euzenir N. Sarno ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Primary Cultures ◽  
Mycobacterium Leprae ◽  
Microbial Pathogens ◽  
Interleukin 4 ◽  
Common Mechanism ◽  
Specific Cell

ABSTRACT The ability of microbial pathogens to target specific cell types is a key aspect of the pathogenesis of infectious disease. Mycobacterium leprae, by infecting Schwann cells, contributes to nerve injury in patients with leprosy. Here, we investigated mechanisms of host-pathogen interaction in the peripheral nerve lesions of leprosy. We found that the expression of the C-type lectin, CD209, known to be expressed on tissue macrophages and to mediate the uptake of M. leprae, was present on Schwann cells, colocalizing with the Schwann cell marker, CNPase (2′,3′-cyclic nucleotide 3′-phosphodiesterase), along with the M. leprae antigen PGL-1 in the peripheral nerve biopsy specimens. In vitro, human CD209-positive Schwann cells, both from primary cultures and a long-term line, have a higher binding of M. leprae compared to CD209-negative Schwann cells. Interleukin-4, known to be expressed in skin lesions from multibacillary patients, increased CD209 expression on human Schwann cells and subsequent Schwann cell binding to M. leprae, whereas Th1 cytokines did not induce CD209 expression on these cells. Therefore, the regulated expression of CD209 represents a common mechanism by which Schwann cells and macrophages bind and take up M. leprae, contributing to the pathogenesis of leprosy.

Essential Role of Src Suppressed C Kinase Substrates in Schwann Cells Adhesion, Spreading and Migration

2008 ◽  
Vol 34 (5) ◽  
pp. 1002-1010 ◽  
Author(s):  
Meijuan Yan ◽  
Chun Cheng ◽  
Jing Jiang ◽  
Yonghua Liu ◽  
Ying Gao ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Essential Role ◽  
And Migration ◽  
Kinase Substrates

Charcot–Marie–Tooth type 4B demyelinating neuropathy: deciphering the role of MTMR phosphatases

2007 ◽  
Vol 9 (25) ◽  
pp. 1-16 ◽  
Author(s):  
Stefano C. Previtali ◽  
Angelo Quattrini ◽  
Alessandra Bolino
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Autosomal Recessive ◽  
Protein Tyrosine Phosphatases ◽  
Vesicular Trafficking ◽  
Demyelinating Neuropathy ◽  
Charcot Marie Tooth ◽  
Catalytically Active ◽  
Tooth Type

AbstractCharcot–Marie–Tooth type 4B (CMT4B) is a severe autosomal recessive neuropathy with demyelination and myelin outfoldings of the nerve. This disorder is genetically heterogeneous, but thus far, mutations in myotubularin-related 2 (MTMR2) and MTMR13 genes have been shown to underlie CMT4B1 and CMT4B2, respectively. MTMR2 and MTMR13 belong to a family of ubiquitously expressed proteins sharing homology with protein tyrosine phosphatases (PTPs). The MTMR family, which has 14 members in humans, comprises catalytically active proteins, such as MTMR2, and catalytically inactive proteins, such as MTMR13. Despite their homology with PTPs, catalytically active MTMR phosphatases dephosphorylate both PtdIns3P and PtdIns(3,5)P2 phosphoinositides. Thus, MTMR2 and MTMR13 may regulate vesicular trafficking in Schwann cells. Loss of these proteins could lead to uncontrolled folding of myelin and, ultimately, to CMT4B. In this review, we discuss recent findings on this interesting protein family with the main focus on MTMR2 and MTMR13 and their involvement in the biology of Schwann cell and CMT4B neuropathies.

scholarly journals SoxD transcription factor deficiency in Schwann cells delays myelination in the developing peripheral nervous system

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ella Ittner ◽  
Anna C. Hartwig ◽  
Olga Elsesser ◽  
Hannah M. Wüst ◽  
Franziska Fröb ◽  
...  
Keyword(s):  
Nervous System ◽  
Schwann Cell ◽  
Peripheral Nervous System ◽  
Schwann Cells ◽  
Terminal Differentiation ◽  
Factor Deficiency ◽  
Schwann Cell Development ◽  
The Central Nervous System ◽  
Brain And Spinal Cord

AbstractThe three SoxD proteins, Sox5, Sox6 and Sox13, represent closely related transcription factors with important roles during development. In the developing nervous system, SoxD proteins have so far been primarily studied in oligodendroglial cells and in interneurons of brain and spinal cord. In oligodendroglial cells, Sox5 and Sox6 jointly maintain the precursor state, interfere with terminal differentiation, and thereby ensure the proper timing of myelination in the central nervous system. Here we studied the role of SoxD proteins in Schwann cells, the functional counterpart of oligodendrocytes in the peripheral nervous system. We show that Schwann cells express Sox5 and Sox13 but not Sox6. Expression was transient and ceased with the onset of terminal differentiation. In mice with early Schwann cell-specific deletion of both Sox5 and Sox13, embryonic Schwann cell development was not substantially affected and progressed normally into the promyelinating stage. However, there was a mild and transient delay in the myelination of the peripheral nervous system of these mice. We therefore conclude that SoxD proteins—in stark contrast to their action in oligodendrocytes—promote differentiation and myelination in Schwann cells.

scholarly journals Biological Role of Dystroglycan in Schwann Cell Function and Its Implications in Peripheral Nervous System Diseases

2010 ◽  
Vol 2010 ◽  
pp. 1-17 ◽  
Author(s):  
Toshihiro Masaki ◽  
Kiichiro Matsumura
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Function ◽  
Cell Polarization ◽  
Targeted Mutagenesis ◽  
Biological Role ◽  
Central Component ◽  
Molecular Architecture ◽  
Loss Of Function

Dystroglycan is a central component of the dystrophin-glycoprotein complex (DGC) that links extracellular matrix with cytoskeleton, expressed in a variety of fetal and adult tissues. Dystroglycan plays diverse roles in development and homeostasis including basement membrane formation, epithelial morphogenesis, membrane stability, cell polarization, and cell migration. In this paper, we will focus on biological role of dystroglycan in Schwann cell function, especially myelination. First, we review the molecular architecture of DGC in Schwann cell abaxonal membrane. Then, we will review the loss-of-function studies using targeted mutagenesis, which have revealed biological functions of each component of DGC in Schwann cells. Based on these findings, roles of dystroglycan in Schwann cell function, in myelination in particular, and its implications in diseases will be discussed in detail. Finally, in view of the fact that understanding the role of dystroglycan in Schwann cells is just beginning, future perspectives will be discussed.

scholarly journals Tissue culture observations relevant to the study of axon-Schwann cell interactions during peripheral nerve development and repair

1987 ◽  
Vol 132 (1) ◽  
pp. 21-34 ◽  
Author(s):  
R. P. Bunge
Keyword(s):  
Tissue Culture ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Basal Lamina ◽  
Heparan Sulphate ◽  
Cell Contact ◽  
Myelinated Nerve ◽  
Nerve Development

During peripheral nerve development the Schwann cell population is expanded so that adequate numbers are available for ensheathment of both nonmyelinated and myelinated nerve fibres. As ensheathment of these fibres progresses each axon--Schwann cell unit becomes surrounded by a basal lamina, providing a unique microtubular framework within the peripheral nerve trunk. Tissue culture studies of pure populations of neurones and Schwann cells cultured separately and in combination indicate that a surface component on the axon provides a mitogenic signal to Schwann cells requiring cell-cell contact. Biochemical, electron microscopic and immunocytochemical analyses of these cultures indicate that Schwann cells in contact with axons are able to generate a basal lamina (containing type IV collagen, laminin and heparan sulphate proteoglycan) and fibrous collagen, without the aid of other cells, and that axonal contact is required for deposition of the basal lamina. The role of Schwann cells and the extracellular matrix they synthesize and organize, as well as the role of the other known products of the Schwann cells in the process of peripheral nerve regeneration, are discussed. It is suggested that the large numbers and advantageous position of the Schwann cells, as well as their ability to provide their own surfaces, a basal lamina and multiple secretory products, may account for their extraordinary ability to foster nerve fibre regeneration.

scholarly journals Leukemia inhibitory factor regulates Schwann cell proliferation and migration and affects peripheral nerve regeneration

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Qianqian Chen ◽  
Qianyan Liu ◽  
Yunsong Zhang ◽  
Shiying Li ◽  
Sheng Yi
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Peripheral Nerves ◽  
Leukemia Inhibitory Factor ◽  
Peripheral Nerve Regeneration ◽  
And Migration ◽  
Proliferation And Migration

AbstractLeukemia inhibitory factor (LIF) is a pleiotropic cytokine that stimulates neuronal development and survival. Our previous study has demonstrated that LIF mRNA is dysregulated in the peripheral nerve segments after nerve injury. Here, we show that LIF protein is abundantly expressed in Schwann cells after rat sciatic nerve injury. Functionally, suppressed or elevated LIF increases or decreases the proliferation rate and migration ability of Schwann cells, respectively. Morphological observations demonstrate that in vivo application of siRNA against LIF after peripheral nerve injury promotes Schwann cell migration and proliferation, axon elongation, and myelin formation. Electrophysiological and behavior assessments disclose that knockdown of LIF benefits the function recovery of injured peripheral nerves. Differentially expressed LIF affects the metabolism of Schwann cells and negatively regulates ERFE (Erythroferrone). Collectively, our observations reveal the essential roles for LIF in regulating the proliferation and migration of Schwann cells and the regeneration of injured peripheral nerves, discover ERFE as a downstream effector of LIF, and extend our understanding of the molecular mechanisms underlying peripheral nerve regeneration.

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