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Journal articles on the topic 'Ependymin'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Rother, Stefan, Rupert Schmidt, Wolfgang Brysch, and Karl-Hermann Schlingensiepen. "Learning-Induced Expression of Meningeal Ependymin mRNA and Demonstration of Ependymin in Neurons and Glial Cells." Journal of Neurochemistry 65, no. 4 (November 23, 2002): 1456–64. http://dx.doi.org/10.1046/j.1471-4159.1995.65041456.x.

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2

SHASHOUA, VICTOR E. "Ependymin, a Brain Extracellular Glycoprotein, and CNS Plasticity." Annals of the New York Academy of Sciences 627, no. 1 Activity-Driv (August 1991): 94–114. http://dx.doi.org/10.1111/j.1749-6632.1991.tb25916.x.

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3

Adams, David S., Miki Kiyokawa, Michael E. Getman, and Victor E. Shashoua. "Genes encoding giant danio and golden shiner ependymin." Neurochemical Research 21, no. 3 (March 1996): 377–84. http://dx.doi.org/10.1007/bf02531655.

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4

Park, Jeong Kuk, Keon Young Kim, Yeo Won Sim, Yong-In Kim, Jin Kyun Kim, Cheol Lee, Jeongran Han, Chae Un Kim, J. Eugene Lee, and SangYoun Park. "Structures of three ependymin-related proteins suggest their function as a hydrophobic molecule binder." IUCrJ 6, no. 4 (June 20, 2019): 729–39. http://dx.doi.org/10.1107/s2052252519007668.

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Ependymin was first discovered as a predominant protein in brain extracellular fluid in fish and was suggested to be involved in functions mostly related to learning and memory. Orthologous proteins to ependymin called ependymin-related proteins (EPDRs) have been found to exist in various tissues from sea urchins to humans, yet their functional role remains to be revealed. In this study, the structures of EPDR1 from frog, mouse and human were determined and analyzed. All of the EPDR1s fold into a dimer using a monomeric subunit that is mostly made up of two stacking antiparallel β-sheets with a curvature on one side, resulting in the formation of a deep hydrophobic pocket. All six of the cysteine residues in the monomeric subunit participate in the formation of three intramolecular disulfide bonds. Other interesting features of EPDR1 include two asparagine residues with glycosylation and a Ca2+-binding site. The EPDR1 fold is very similar to the folds of bacterial VioE and LolA/LolB, which also use a similar hydrophobic pocket for their respective functions as a hydrophobic substrate-binding enzyme and a lipoprotein carrier, respectively. A further fatty-acid binding assay using EPDR1 suggests that it indeed binds to fatty acids, presumablyviathis pocket. Additional interactome analysis of EPDR1 showed that EPDR1 interacts with insulin-like growth factor 2 receptor and flotillin proteins, which are known to be involved in protein and vesicle translocation.

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5

Anderson, Marilyn J., Chi Y. Choy, and Stephen G. Waxman. "Selforganization of ependyma in regenerating teleost spinal cord: evidence from serial section reconstructions." Development 96, no. 1 (July 1, 1986): 1–18. http://dx.doi.org/10.1242/dev.96.1.1.

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Multiple ependymal structures have been observed in regenerating spinal cord of the teleost Apteronotus albifrons. Evidence is presented for two modes of formation of the secondary ependymas: budding off from the primary ependyma, and de novo origin of a tube-like ependymal structure within a group of undifferentiated cells. Serial sections of regenerated cord provide evidence that undifferentiated cells not in immediate contact with the main ependymal layer can organize and differentiate into an ependymal structure in the regenerating spinal cord. These findings suggest that a significant amount of morphological organization can take place independent of the normal developmental sequence and environment.

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6

Suárez-Castillo, Edna C., and José E. García-Arrarás. "Deciphering the molecular evolution of the ependymin protein family." Developmental Biology 295, no. 1 (July 2006): 424. http://dx.doi.org/10.1016/j.ydbio.2006.04.304.

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7

Königstorfer, A., S. Sterrer, C. Eckerskorn, F. Lottspeich, R. Schmidt, and W. Hoffmann. "Molecular Characterization of an Ependymin Precursor from Goldfish Brain." Journal of Neurochemistry 52, no. 1 (January 1989): 310–12. http://dx.doi.org/10.1111/j.1471-4159.1989.tb10932.x.

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8

Adams, David S., and Victor E. Shashoua. "Cloning and sequencing the genes encoding goldfish and carp ependymin." Gene 141, no. 2 (April 1994): 237–41. http://dx.doi.org/10.1016/0378-1119(94)90578-9.

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9

Sterrer, S., A. Königstorfer, and W. Hoffman. "Biosynthesis and expression of ependymin homologous sequences in zebrafish brain." Neuroscience 37, no. 1 (January 1990): 277–84. http://dx.doi.org/10.1016/0306-4522(90)90214-o.

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10

Park, SangYoun. "De novo Phasing Xenons Observed in the Frog Ependymin-Related Protein." Crystals 10, no. 1 (January 10, 2020): 32. http://dx.doi.org/10.3390/cryst10010032.

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Pressurizing Xe or Kr noble gas into the protein crystal for de novo phasing has been one method of choice when the introduction of other heavy-atom compounds fails. One reason is because, unlike other heavy-atom compounds, their immobilized sites are mostly hydrophobic cavities. Previously, the structure of frog ependymin-related protein (EPDR) has been determined using a single wavelength anomalous diffraction (SAD) on a Xe-pressurized crystal. Since no report on the four Xe binding sites has been made, these sites are analyzed in this study. Of the four Xe atoms, three are found along the hydrophobic interfaces created by the two crystallographic symmetry mates of EPDR. One final Xe atom occupies a Ca2+-binding site of the native protein entirely stabilized by the polar atoms of the surrounding EDPR residues. We believe that this atypical Xe location is very unique and merits further study.

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11

Gregorio-King, Claudia C., Janet L. McLeod, Fiona McL Collier, Gregory R. Collier, Karyn A. Bolton, Gavin J. Van Der Meer, Jim Apostolopoulos, and Mark A. Kirkland. "MERP1: a mammalian ependymin-related protein gene differentially expressed in hematopoietic cells." Gene 286, no. 2 (March 2002): 249–57. http://dx.doi.org/10.1016/s0378-1119(02)00434-1.

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12

Sneddon, Lynne U., Rupert Schmidt, Yongxiang Fang, and Andrew R. Cossins. "Molecular Correlates of Social Dominance: A Novel Role for Ependymin in Aggression." PLoS ONE 6, no. 4 (April 5, 2011): e18181. http://dx.doi.org/10.1371/journal.pone.0018181.

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13

Shashoua, V. E., G. W. Hesse, and B. Milinazzo. "Evidence for the in vivo polymerization of ependymin: a brain extracellular glycoprotein." Brain Research 522, no. 2 (July 1990): 181–90. http://dx.doi.org/10.1016/0006-8993(90)91460-x.

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14

Tang, Shye-Jye, Kuang-Hui Sun, Guang-Huan Sun, Guang Lin, Wen-Wen Lin, and Mei-Jan Chuang. "Cold-induced ependymin expression in zebrafish and carp brain: implications for cold acclimation." FEBS Letters 459, no. 1 (September 27, 1999): 95–99. http://dx.doi.org/10.1016/s0014-5793(99)01229-6.

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15

Nimmrich, Inko, Silke Erdmann, Ute Melchers, Slava Chtarbova, Ulrich Finke, Sebastian Hentsch, Ingrid Hoffmann, Martin Oertel, Werner Hoffmann, and Oliver Müller. "The novel ependymin related gene UCC1 is highly expressed in colorectal tumor cells." Cancer Letters 165, no. 1 (April 2001): 71–79. http://dx.doi.org/10.1016/s0304-3835(01)00390-1.

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16

Park, Jeong Kuk, and SangYoun Park. "A Single Soaked Iridium ( IV ) Ion Observed in the Frog Ependymin‐Related Protein." Bulletin of the Korean Chemical Society 41, no. 8 (August 2020): 778–81. http://dx.doi.org/10.1002/bkcs.12080.

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17

Schmidt, John T., and Victor E. Shashoua. "Antibodies to ependymin block the sharpening of the regenerating retinotectal projection in goldfish." Brain Research 446, no. 2 (April 1988): 269–84. http://dx.doi.org/10.1016/0006-8993(88)90886-4.

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18

Shashoua, V. E., and G. W. Hesse. "Classical conditioning leads to changes in extracellular concentrations of ependymin in goldfish brain." Brain Research 484, no. 1-2 (April 1989): 333–39. http://dx.doi.org/10.1016/0006-8993(89)90377-6.

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19

Schmidt, John T., Rupert Schmidt, Weichun Lin, Xiaoying Jian, and Claudia A. O. Stuermer. "Ependymin as a substrate for outgrowth of axons from cultured explants of goldfish retina." Journal of Neurobiology 22, no. 1 (January 1991): 40–54. http://dx.doi.org/10.1002/neu.480220105.

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20

Orti, G., and A. Meyer. "Molecular evolution of ependymin and the phylogenetic resolution of early divergences among euteleost fishes." Molecular Biology and Evolution 13, no. 4 (April 1, 1996): 556–73. http://dx.doi.org/10.1093/oxfordjournals.molbev.a025616.

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21

Park, Jeong, Yeo Sim, and SangYoun Park. "Over-Expression, Secondary Structure Characterization, and Preliminary X-ray Crystallographic Analysis of Xenopus tropicalis Ependymin." Crystals 8, no. 7 (July 11, 2018): 284. http://dx.doi.org/10.3390/cryst8070284.

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22

Schmidt, Rupert, Wolfgang Brysch, Stefan Rother, and Karl-Hermann Schlingensiepen. "Inhibition of Memory Consolidation After Active Avoidance Conditioning by Antisense Intervention with Ependymin Gene Expression." Journal of Neurochemistry 65, no. 4 (November 23, 2002): 1465–71. http://dx.doi.org/10.1046/j.1471-4159.1995.65041465.x.

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23

Shashoua, Victor E. "Monomeric and polymeric forms of ependymin: A brain extracellular glycoprotein implicated in memory consolidation processes." Neurochemical Research 13, no. 7 (July 1988): 649–55. http://dx.doi.org/10.1007/bf00973283.

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24

Banker, Piyush, Smitha Sonni, Ilya Kister, John P. Loh, and Yvonne W. Lui. "Pencil-thin ependymal enhancement in neuromyelitis optica spectrum disorders." Multiple Sclerosis Journal 18, no. 7 (December 19, 2011): 1050–53. http://dx.doi.org/10.1177/1352458511431730.

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AQP4 water channels are thought to be the target of autoimmune attack in neuromyelitis optica-spectrum disorders (NMOsd). AQP4 are highly expressed on ventricular ependyma. The objective of this study was to describe a novel pattern of linear, ‘pencil-thin’ enhancement of ventricular ependyma in NMOsd. We report two NMOsd patients with pencil-thin ependymal enhancement along the frontal and occipital horns of lateral ventricles. Differential diagnosis of ependymal enhancement should include NMOsd alongside with infectious and neoplastic etiologies. Pencil-thin ependymal enhancement may be a helpful radiological marker of NMOsd that can be used to differentiate this condition from multiple sclerosis.

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25

Piront, Marie-Luise, and Rupert Schmidt. "Inhibition of long-term memory formation by anti-ependymin antisera after active shock-avoidance learning in goldfish." Brain Research 442, no. 1 (February 1988): 53–62. http://dx.doi.org/10.1016/0006-8993(88)91431-x.

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26

Abouhamed, Marouan, Kay Grobe, Isabelle V. Leefa Chong San, Sabine Thelen, Ulrike Honnert, Maria S. Balda, Karl Matter, and Martin Bähler. "Myosin IXa Regulates Epithelial Differentiation and Its Deficiency Results in Hydrocephalus." Molecular Biology of the Cell 20, no. 24 (December 15, 2009): 5074–85. http://dx.doi.org/10.1091/mbc.e09-04-0291.

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The ependymal multiciliated epithelium in the brain restricts the cerebrospinal fluid to the cerebral ventricles and regulates its flow. We report here that mice deficient for myosin IXa (Myo9a), an actin-dependent motor molecule with a Rho GTPase–activating (GAP) domain, develop severe hydrocephalus with stenosis and closure of the ventral caudal 3rd ventricle and the aqueduct. Myo9a is expressed in maturing ependymal epithelial cells, and its absence leads to impaired maturation of ependymal cells. The Myo9a deficiency further resulted in a distorted ependyma due to irregular epithelial cell morphology and altered organization of intercellular junctions. Ependymal cells occasionally delaminated, forming multilayered structures that bridged the CSF-filled ventricular space. Hydrocephalus formation could be significantly attenuated by the inhibition of the Rho-effector Rho-kinase (ROCK). Administration of ROCK-inhibitor restored maturation of ependymal cells, but not the morphological distortions of the ependyma. Similarly, down-regulation of Myo9a by siRNA in Caco-2 adenocarcinoma cells increased Rho-signaling and induced alterations in differentiation, cell morphology, junction assembly, junctional signaling, and gene expression. Our results demonstrate that Myo9a is a critical regulator of Rho-dependent and -independent signaling mechanisms that guide epithelial differentiation. Moreover, Rho-kinases may represent a new target for therapeutic intervention in some forms of hydrocephalus.

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27

RINDER, HEINZ, THOMAS A. BAYER, EVA-MARIA GERTZEN, and WERNER HOFFMANN. "Molecular Analysis of the Ependymin Gene and Functional Test of Its Promoter Region by Transient Expression in Brachydanio rerio." DNA and Cell Biology 11, no. 6 (July 1992): 425–32. http://dx.doi.org/10.1089/dna.1992.11.425.

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28

Apostolopoulos, Jim, Rosemary L. Sparrow, Janet L. McLeod, Fiona M. Collier, Phil K. Darcy, Howard R. Slater, Con Ngu, Claudia C. Gregorio-King, and Mark A. Kirkland. "Identification and Characterization of a Novel Family of Mammalian Ependymin-Related Proteins (MERPs) in Hematopoietic, Nonhematopoietic, and Malignant Tissues." DNA and Cell Biology 20, no. 10 (October 2001): 625–35. http://dx.doi.org/10.1089/104454901753340613.

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29

Suárez-Castillo, Edna C., Wanda E. Medina-Ortı́z, José L. Roig-López, and José E. Garcı́a-Arrarás. "Ependymin, a gene involved in regeneration and neuroplasticity in vertebrates, is overexpressed during regeneration in the echinoderm Holothuria glaberrima." Gene 334 (June 2004): 133–43. http://dx.doi.org/10.1016/j.gene.2004.03.023.

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30

Hirst, Robert A., Bashir J. Mohammed, Timothy J. Mitchell, Peter W. Andrew, and Christopher O'Callaghan. "Streptococcus pneumoniae-Induced Inhibition of Rat Ependymal Cilia Is Attenuated by Antipneumolysin Antibody." Infection and Immunity 72, no. 11 (November 2004): 6694–98. http://dx.doi.org/10.1128/iai.72.11.6694-6698.2004.

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ABSTRACT Ciliated ependymal cells line the ventricular surfaces and aqueducts of the brain. In ex vivo experiments, pneumolysin caused rapid inhibition of the ependymal ciliary beat frequency and caused ependymal cell disruption. Wild-type pneumococci and pneumococci deficient in pneumolysin caused ciliary slowing, but penicillin lysis of wild-type, not pneumolysin-deficient, pneumococci increased the extent of ciliary inhibition. This effect was abolished by antipneumolysin antibody. Ependymal ciliary stasis by purified pneumolysin was also blocked by the addition of antipneumolysin monoclonal antibodies. These data show that antibiotic lysis of Streptococcus pneumoniae can be detrimental to the ciliated ependyma and that antipneumolysin antibody may have a therapeutic potential.

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31

Valle, Maria Cecilia Della, David E. Sleat, Istvan Sohar, Ting Wen, John E. Pintar, Michel Jadot, and Peter Lobel. "Demonstration of Lysosomal Localization for the Mammalian Ependymin-related Protein Using Classical Approaches Combined with a Novel Density Shift Method." Journal of Biological Chemistry 281, no. 46 (September 5, 2006): 35436–45. http://dx.doi.org/10.1074/jbc.m606208200.

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32

Hirst, Robert A., Bejal Gosai, Andrew Rutman, Peter W. Andrew, and Christopher O'Callaghan. "Streptococcus pneumoniae Damages the Ciliated Ependyma of the Brain during Meningitis." Infection and Immunity 71, no. 10 (October 2003): 6095–100. http://dx.doi.org/10.1128/iai.71.10.6095-6100.2003.

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ABSTRACT Streptococcus pneumoniae meningitis remains a disease with a poor outcome for the patient. A region of the brain that has been neglected in the study of meningitis is the ependyma, which has been identified as a location of adult pluripotent cells. In this study we have used a rat model of meningitis to examine whether the ependymal layer is affected by S. pneumoniae. The effects included localized loss of cilia, a decrease of the overall ependymal ciliary beat frequency, and damage to the ependymal ultrastructure during meningitis. In conclusion, loss of ependymal cells and ciliary function exposes the underlying neuronal milieu to host and bacterial cytotoxins and this is likely to contribute to the neuropathology commonly observed in pneumococcal meningitis.

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33

Sharma, Sumit, Shashi Kant Jain, and Virendra Deo Sinha. "Use of Preoperative Ependymal Enhancement on Magnetic Resonance Imaging Brain as a Marker of Grade of Glioma." Journal of Neurosciences in Rural Practice 08, no. 04 (October 2017): 545–50. http://dx.doi.org/10.4103/jnrp.jnrp_78_17.

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ABSTRACT Objectives: Neural stem cells within the subventricular zone (SVZ) are thought to be responsible for the origin and the heterogeneous nature of the gliomas. The relationship of the gliomas to the SVZ can be appreciated as ependymal enhancement on contrast magnetic resonance imaging (MRI). This study evaluates the rate of ependymal enhancement and its association with the histopathological grade of gliomas. Patients and Methods: Seventy-five patients with radiological features of glioma were recruited. Preoperative MRI was evaluated for the presence of ependymal enhancement and fluid-attenuated inversion recovery (FLAIR) signal proximity of tumor to ependyma, and the association to grade was investigated. Results: Seventy-five patients studied showed a male predominance (62.66%) with a mean age of 44.91 ± 13.64 years. Evidence of ependymal enhancement was positive in 24% (n =; 18), 46.67% (n =; 35) showed no evidence, and in 29.33% (n =; 22), assessment was inconclusive. According to WHO grading, 76% (n =; 57) were high-grade gliomas (HGGs) including Grade III (n =; 17) and Grade IV (n =; 40) and 24% (n =; 18) were low-grade gliomas (LGGs) Grade II. HGGs were significantly associated with ependymal enhancement (P< 0.01) and FLAIR signal proximity to the ependyma (P< 0.001). Among HGGs, rate of ependymal enhancement and FLAIR signal proximity was more in Grade IV than Grade III but was not statistically significant (P > 0.05). Conclusion: SVZ is associated with HGGs. These MRI features can be helpful in predicting the tumor grade preoperatively and by including LGGs, the role of SVZ in the heterogeneous disease process of glioma can be studied as a whole, not only in the glioblastoma (GBM).

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34

Milhorat, Thomas H., and René M. Kotzen. "Stenosis of the central canal of the spinal cord following inoculation of suckling hamsters with reovirus type I." Journal of Neurosurgery 81, no. 1 (July 1994): 103–6. http://dx.doi.org/10.3171/jns.1994.81.1.0103.

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✓ The central canal of the human spinal cord is partially or completely occluded in the vast majority of individuals by the early years of adult life. The authors describe an experimental lesion following virus-induced ependymitis that bears a striking resemblance to the condition in man. Suckling hamsters were inoculated with 0.06 ml of 10−3 infectivity titer of reovirus type I between the 2nd and 5th days of life. The pathological events consisted of necrotizing ependymitis, healing of the ependyma by gliovascular scarring, and obstruction of narrow bottlenecks such as the central canal. Histological findings were characterized by disorganization of the ependyma, formation of ependymal rosettes and microtubules, subependymal gliovascular scarring, and intracanalicular gliosis. These features are the same as those encountered clinically and provide strong evidence that stenosis of the central canal in man is a pathological lesion involving ependymal injury and scarring.

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35

Rosenberg, G. A., W. T. Kyner, J. D. Fenstermacher, and C. S. Patlak. "Effect of vasopressin on ependymal and capillary permeability to tritiated water in cat." American Journal of Physiology-Renal Physiology 251, no. 3 (September 1, 1986): F485—F489. http://dx.doi.org/10.1152/ajprenal.1986.251.3.f485.

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Ependymal cells line the cerebral ventricles forming the interface that separates the cerebrospinal (CSF) and interstitial fluids (ISF). Extracellular molecules move between ependymal cells, whereas lipid soluble molecules pass both between and through cells. We measured the transfer of tritiated water (TOH) from CSF to blood across the ependymal and capillary interfaces by ventriculocisternal (VC) steady-state tissue clearance. Adult cats anesthetized with pentobarbital sodium underwent VC perfusion with the extracellular marker [14C]sucrose and TOH added to the artificial CSF. Brain tissue was analyzed for depth of penetration of the isotopes into periventricular gray matter. We found that TOH distribution space was lower than expected from water content measurements, whereas sucrose space was normal. Using VC steady-state equations we calculated an ependymal permeability that was similar to the permeability of the cerebral capillary. When arginine vasopressin (AVP) was added to the perfusate in different amounts, both capillary transfer times and ependymal permeability increased. Our results show that the ependyma may be important in water movement in the brain and support the suggestion that AVP influences water exchange in mammalian brain tissue.

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36

Del Bigio, Marc R., J. Edward Bruni, and H. Derek Fewer. "Human neonatal hydrocephalus." Journal of Neurosurgery 63, no. 1 (July 1985): 56–63. http://dx.doi.org/10.3171/jns.1985.63.1.0056.

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✓ An infant of 43 weeks gestational age with severe congenital hydrocephalus was operated on for removal of a subependymal astrocytoma in the region of the foramen of Monro. A biopsy of periventricular tissue was taken from the lateral ventricle for examination by scanning and transmission electron microscopy. The ependyma was largely denuded, with glial cell processes forming most of the ventricular lining. Many of the attenuated ependymal cells, however, had intact junctional complexes at areas of contact with other ependymal cells. Club-shaped unipolar cells, believed to be a previously undescribed form of immature ependymal cells, were found in the ventricular lining. Cerebrospinal fluid edema was present in the neuropil up to 60 µm from the ventricular lumen, but there was no obvious axonal pathology in the tissues examined.

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37

Romero, Flávio Ramalho, Marco Antônio Zanini, Luis Gustavo Ducati, Roberto Bezerra Vital, Newton Moreira de Lima Neto, and Roberto Colichio Gabarra. "Purely Cortical Anaplastic Ependymoma." Case Reports in Oncological Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/541431.

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Ependymomas are glial tumors derived from ependymal cells lining the ventricles and the central canal of the spinal cord. It may occur outside the ventricular structures, representing the extraventicular form, or without any relationship of ventricular system, called ectopic ependymona. Less than fifteen cases of ectopic ependymomas were reported and less than five were anaplastic. We report a rare case of pure cortical ectopic anaplastic ependymoma.

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38

Zheng, Fa-Xin, Xiu-Qin Sun, Bao-Hai Fang, Xu-Guang Hong, and Jin-Xing Zhang. "Comparative analysis of genes expressed in regenerating intestine and non-eviscerated intestine of Apostichopus japonicus Selenka (Aspidochirotida: Stichopodidae) and cloning of ependymin gene." Hydrobiologia 571, no. 1 (July 13, 2006): 109–22. http://dx.doi.org/10.1007/s10750-006-0231-z.

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39

Sarnat, Harvey B. "Regional Ependymal Upregulation of Vimentin in Chiari II Malformation, Aqueductal Stenosis, and Hydromyelia." Pediatric and Developmental Pathology 7, no. 1 (January 2004): 48–60. http://dx.doi.org/10.1007/s10024-003-2127-5.

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Vimentin, glial fibrillary acidic protein (GFAP) and S-100β protein were studied by immunocytochemistry in the ependyma of patients with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia. Paraffin sections of brains and spinal cords of 16 patients were examined, 14 with Chiari II malformations, most with aqueductal stenosis and/or hydromyelia as associated features, and 2 patients with congenital aqueductal stenosis without Chiari malformation. Patients ranged in age from 20-wk gestation to 48 years. The results demonstrated: 1) in the fetus and young infant with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia, vimentin is focally upregulated in the ependyma only in areas of dysgenesis and not in the ependyma throughout the ventricular system; 2) GFAP and S-100β protein are not coexpressed, indicating that the selective upregulation of vimentin is not simple maturational delay; 3) vimentin upregulation also is seen in the ependymal remnants of the congenital atretic cerebral aqueduct, not associated with Chiari malformation; 4) in the older child and adult with Chiari II malformation, vimentin overexpression in the ependyma becomes more generalized in the lateral ventricles as well, hence evolves into a nonspecific upregulation. The interpretation from these findings leads to speculation that it is unlikely that ependymal vimentin is directly involved in the pathogenesis of Chiari II malformation, but may reflect a secondary upregulation due to defective expression of another gene. This gene may be one of rhombomeric segmentation that also plays a role in defective programming of the paraxial mesoderm for the basioccipital and supraoccipital bones resulting in a small posterior fossa. This interpretation supports the hypothesis of a molecular genetic defect, rather than a mechanical cause, as the etiology of the Chiari II malformation.

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40

STAHL, W., and Y. KANEDA. "Pathogenesis of murine toxoplasmic hydrocephalus." Parasitology 114, no. 3 (March 1997): 219–29. http://dx.doi.org/10.1017/s0031182096008505.

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The prevailing hypothesis concerning the pathogenesis of toxoplasmic hydrocephalus alleges that (a) parasites invade and destroy the ependymal lining of the lateral ventricles, followed by (b) the sloughing of masses of degenerating ependymal and inflammatory cells leading to obstruction of the ventricular foramina and aqueduct of Sylvius, thereby initiating the hydrocephalus. Our observations in chronically infected mice indicate otherwise. Parasite invasion of the ependyma was not detected; the intraventricular masses of cellular ‘debris’ contained neither ependymal nor inflammatory cells; and obstruction of the ventricular foramina and/or aqueduct was not seen. As an alternative hypothesis, we suggest the development of hydrocephalus in the infected mice was consequent to severe leptomeningeal inflammation blocking the subarachnoid space and impeding the resorption of cerebrospinal fluid by the arachnoid villi. Narrowing of the aqueduct of Sylvius, when present, was adjudged the result, not the cause of the hydrocephalus, due to compression of the midbrain by the enlarging lateral ventricles.

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41

Shashoua, Victor E., David Adams, and Anne Boyer-Boiteau. "CMX-8933, a peptide fragment of the glycoprotein ependymin, promotes activation of AP-1 transcription factor in mouse neuroblastoma and rat cortical cell cultures." Neuroscience Letters 312, no. 2 (October 2001): 103–7. http://dx.doi.org/10.1016/s0304-3940(01)02119-x.

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Del Bigio, Marc R., and J. Edward Bruni. "Reaction of rabbit lateral periventricular tissue to shunt tubing implants." Journal of Neurosurgery 64, no. 6 (June 1986): 932–40. http://dx.doi.org/10.3171/jns.1986.64.6.0932.

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✓ The reaction of the periventricular tissue of the lateral ventricle to silicone rubber shunt tubing was studied by scanning and transmission electron microscopy. Nonfunctioning shunt tubing was implanted bilaterally into the frontal horns of rabbits, which were then sacrificed at postoperative intervals of 3 days to 16 weeks. Colchicine was used to study mitotic activity at the 3-day to 4-week postimplantation intervals. Reactive changes that occurred in the periventricular tissue correlated with the degree of contact with the implant and also with the duration of the postoperative period. Ependymal cells underwent progressive attenuation and sloughed completely in the most severely affected areas. Prominent gliosis in the subependyma accompanied the ependymal changes. The ventricular surface directly adjacent to holes in the implant developed ependyma-covered glial evaginations which grew into the implant holes beginning 1 week postimplantation. In the region of the outgrowths, ependymal mitotic activity was significantly increased at 1 and 2 weeks postimplantation, and astroglial mitotic activity was increased at 3 days and 1 week. Proliferation of ependymal and glial cells in the area touching the shunt tubing and mechanical factors contributed to the development of cellular outgrowths which may be a factor in the pathogenesis of shunt obstruction in human hydrocephalus.

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43

Olude, M. A., F. E. Olopade, O. A. Mustapha, S. T. Bello, A. O. Ihunwo, J. Plendl, and J. O. Olopade. "Ultrastructural Morphology of the Ependyma and Choroid Plexus in the African Giant Rat (Cricetomys gambianus)." Folia Veterinaria 65, no. 1 (March 1, 2021): 45–53. http://dx.doi.org/10.2478/fv-2021-0006.

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Abstract Ependymal cells line the interface between the ventricular surfaces and the brain parenchyma. These cells, in addition to the choroid plexus, form the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) and serve important functions in the protection and regulation of brain metabolism. The African giant rat (AGR) has been used as sentinels to detect potential neuropathology arising from ecotoxicological pollutions. This study examined the lateral ventricular lining by using histology, immunohistochemistry and electron microscopy. Marked variations were observed in some regions of the ventricles which showed multi-layering of ependymal cells that differed from the typical single layered ependymal cells at the apical surface, while subependymal structures revealed indistinctive neuropil and glia following histological examinations. The ependymal cells which form the epithelial lining of the ventricles were comprised of cuboidal or low columnar cells, with the plasmalemma of abutting cells forming intercellular bridge appearing links by: tight junctions (zonula occludens), intermediate junctions (zonula adherens), desmosomes (macula adherens) and infrequent gap junctions. The choroid plexus revealed cells of Kolmer with several cilia and microvilli. The possible functional components of the ependyma and choroid plexus morphology of the AGR are discussed and thus provide a baseline for further research on the AGR brain.

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Shashoua, Victor E., P. M. Nolan, T. B. Shea, and B. Milinazzo. "Dibutyryl cyclic AMP stimulates expression of ependymin mRNA and the synthesis and release of the protein into the culture medium by neuroblastoma cells (NB2a/d1)." Journal of Neuroscience Research 32, no. 2 (June 1992): 239–44. http://dx.doi.org/10.1002/jnr.490320213.

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Znalesniak, Eva B., Ting Fu, Karina Guttek, Ulrike Händel, Dirk Reinhold, and Werner Hoffmann. "Increased Cerebral Tff1 Expression in Two Murine Models of Neuroinflammation." Cellular Physiology and Biochemistry 39, no. 6 (2016): 2287–96. http://dx.doi.org/10.1159/000447921.

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Background/Aims: The trefoil factor family (TFF) peptide TFF1 is a typical secretory product of the gastric mucosa and a very low level of expression occurs in nearly all regions of the murine brain. TFF1 possesses a lectin activity and binding to a plethora of transmembrane glycoproteins could explain the diverse biological effects of TFF1 (e.g., anti-apoptotic effect). It was the aim to test whether TFF expression is changed during neuroinflammation. Methods: Expression profiling was performed using semi-quantitative RT-PCR analyses in two murine models of neuroinflammation, i.e. Toxoplasma gondii-induced encephalitis and experimental autoimmune encephalomyelitis (EAE), the latter being the most common animal model of multiple sclerosis. Tff1 expression was also localized using RNA in situ hybridization histochemistry. Results: We report for the first time on a significant transcriptional induction in cerebral Tff1 expression in both T. gondii-induced encephalitis and EAE. In contrast, Tff2 and Tff3 expression were not altered. Tff1 transcripts were predominantly localized in the internal granular layer of the cerebellum indicating neuronal expression. Furthermore, also glial cells are expected to express Tff1. Characterization of both experimental models by expression profiling (e.g., inflammasome sensors, inflammatory cytokines, microglial marker Iba1, ependymin related protein 1) revealed differences concerning the expression of the inflammasome sensor Nlrp1 and interleukin 17a. Conclusion: The up-regulated expression of Tff1 is probably the result of a complex inflammatory process as its expression is induced by tumor necrosis factor α as well as interleukins 1β and 17. However on the transcript level, Tff1KO mice did not show any significant signs of an altered immune response after infection with T. gondii in comparison with the wild type animals.

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Chu, Chun-Ho, Shih-Ching Chang, Hsiu-Hua Wang, Shung-Haur Yang, Kuo-Chu Lai, and Te-Chang Lee. "Prognostic Values of EPDR1 Hypermethylation and Its Inhibitory Function on Tumor Invasion in Colorectal Cancer." Cancers 10, no. 10 (October 22, 2018): 393. http://dx.doi.org/10.3390/cancers10100393.

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Aberrant DNA methylation is a potential mechanism underlying the development of colorectal cancer (CRC). Thus, identification of prognostic DNA methylation markers and understanding the related molecular functions may offer a new perspective on CRC pathogenesis. To that end, we explored DNA methylation profile changes in CRC subtypes based on the microsatellite instability (MSI) status through genome-wide DNA methylation profiling analysis. Of 34 altered genes, three hypermethylated (epidermal growth factor, EGF; carbohydrate sulfotransferase 10, CHST10; ependymin related 1, EPDR1) and two hypomethylated (bone marrow stromal antigen 2, BST2; Rac family small GTPase 3, RAC3) candidates were further validated in CRC patients. Based on quantitative methylation-specific polymerase chain reaction (Q-MSP), EGF, CHST10 and EPDR1 showed higher hypermethylated levels in CRC tissues than those in adjacent normal tissues, whereas BST2 showed hypomethylation in CRC tissues relative to adjacent normal tissues. Additionally, among 75 CRC patients, hypermethylation of CHST10 and EPDR1 was significantly correlated with the MSI status and a better prognosis. Moreover, EPDR1 hypermethylation was significantly correlated with node negativity and a lower tumor stage as well as with mutations in B-Raf proto-oncogene serine/threonine kinase (BRAF) and human transforming growth factor beta receptor 2 (TGFβR2). Conversely, a negative correlation between the mRNA expression and methylation levels of EPDR1 in CRC tissues and cell lines was observed, revealing that DNA methylation has a crucial function in modulating EPDR1 expression in CRC cells. EPDR1 knockdown by a transient small interfering RNA significantly suppressed invasion by CRC cells, suggesting that decreased EPDR1 levels may attenuate CRC cell invasion. These results suggest that DNA methylation-mediated EPDR1 epigenetic silencing may play an important role in preventing CRC progression.

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Jiménez, Antonio J., María-Dolores Domínguez-Pinos, María M. Guerra, Pedro Fernández-Llebrez, and José-Manuel Pérez-Fígares. "Structure and function of the ependymal barrier and diseases associated with ependyma disruption." Tissue Barriers 2, no. 1 (January 2014): e28426. http://dx.doi.org/10.4161/tisb.28426.

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Summy-Long, Joan Y., and Sanmei Hu. "Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 5 (November 2009): R1532—R1545. http://dx.doi.org/10.1152/ajpregu.00340.2009.

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During the brain's innate immune response microglia, astroglia and ependymal cells resolve/repair damaged tissue and control infection. Released interleukin-1β (IL-1β) reaching cerebroventricles stimulates circumventricular organs (CVOs; subfornical organ, SFO; organum vasculosum lamina terminalis, OVLT), the median preoptic nucleus (MePO), and magnocellular and parvocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei. Hypertonic saline (HS) also activates these osmosensory CVOs and neuroendocrine systems, but, in contrast to IL-1β, inhibits the peripheral immune response. To examine whether the brain's innate immune response is attenuated by osmotic stimulation, sterile acidic perfusion fluid was microdialyzed (2 μl/min) in the SON area of conscious rats for 6 h with sterile HS (1.5 M NaCl) injected subcutaneously (15 ml/kg) at 5 h. Immunohistochemistry identified cytokine sources (IL-1β+; OX-42+ microglia) and targets (IL-1R+; inducible cyclooxygenase, COX-2+; c-Fos+) near the probe, in CVOs, MePO, ependymal cells, periventricular hypothalamus, SON, and PVN. Inserting the probe stimulated magnocellular neurons (c-Fos+; SON; PVN) via the MePO (c-Fos+), a response enhanced by HS. Microdialysis activated microglia (OX-42+; amoeboid/hypertrophied; IL-1β+) in the adjacent SON and bilaterally in perivascular areas of the PVN, periventricular hypothalamus and ependyma, coincident with c-Fos expression in ependymal cells and COX-2 in the vasculature. These microglial responses were attenuated by HS, coincident with activating parvocellular and magnocellular neuroendocrine systems and elevating circulating IL-1β, oxytocin, and vasopressin. Acidosis-induced cellular injury from microdialysis activated the brain's innate immune response by a mechanism inhibited by peripheral osmotic stimulation.

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Reddy, Kesava K. V., Marc R. Del Bigio, and Garnette R. Sutherland. "Ultrastructure of the human posttraumatic syrinx." Journal of Neurosurgery 71, no. 2 (August 1989): 239–43. http://dx.doi.org/10.3171/jns.1989.71.2.0239.

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✓ Although posttraumatic syringomyelia is a well-established clinicopathological entity, there is a paucity of information on the ultrastructural features of this condition. This study documents the light and electron microscopic features of posttraumatic syringes obtained from two patients who underwent surgical cordectomy. The syringes were lined largely by cell processes of astrocytes. Small regions near the caudal end were lined by flattened ependymal cells that lacked surface specializations. These were thought to represent remnants of the central canal ependyma. The ultrastructural appearance of the syrinx was similar to that of the communicating syringomyelia as well as the periventricular changes that accompany hydrocephalus. The authors conclude that the changes represent the nonspecific sequelae of a distensile force within the syrinx cavity.

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Roales-Buján, Ruth, Patricia Páez, Montserrat Guerra, Sara Rodríguez, Karin Vío, Ailec Ho-Plagaro, María García-Bonilla, et al. "Astrocytes acquire morphological and functional characteristics of ependymal cells following disruption of ependyma in hydrocephalus." Acta Neuropathologica 124, no. 4 (May 11, 2012): 531–46. http://dx.doi.org/10.1007/s00401-012-0992-6.

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