scholarly journals Wnt signal modulates proliferation of spinal cord ependymal cells by promoting morphological change of the source cells

2017 ◽  
Vol 145 ◽  
pp. S152
Author(s):  
Takuma Shinozuka ◽  
Ritsuko Takada ◽  
Shinji Takada
Keyword(s):  
Spinal Cord ◽  
Morphological Change ◽  
Ependymal Cells ◽  
Wnt Signal

scholarly journals Olig2-positive progenitors in the embryonic spinal cord give rise not only to motoneurons and oligodendrocytes, but also to a subset of astrocytes and ependymal cells

2006 ◽  
Vol 293 (2) ◽  
pp. 358-369 ◽  
Author(s):  
Noritaka Masahira ◽  
Hirohide Takebayashi ◽  
Katsuhiko Ono ◽  
Keisuke Watanabe ◽  
Lei Ding ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ependymal Cells ◽  
Embryonic Spinal Cord

Proliferation and Differentiation of Ependymal Cells after Transection of the Carp Spinal Cord

1997 ◽  
Vol 14 (2) ◽  
pp. 331-338 ◽  
Author(s):  
Hajime Yamada ◽  
Toshihiko Miyake ◽  
Tadahisa Kitamura
Keyword(s):  
Spinal Cord ◽  
Ependymal Cells ◽  
Proliferation And Differentiation

scholarly journals Reaction of ependymal cells to spinal cord injury: a potential role for oncostatin pathway and microglial cells

2021 ◽  
Author(s):  
R. Chevreau ◽  
H Ghazale ◽  
C Ripoll ◽  
C Chalfouh ◽  
Q Delarue ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Glial Cells ◽  
Mapk Signaling ◽  
Central Canal ◽  
Microglial Cells ◽  
Ependymal Cells ◽  
Rna Profiling ◽  
Cord Injury

AbstractEpendymal cells with stem cell properties reside in the adult spinal cord around the central canal. They rapidly activate and proliferate after spinal cord injury, constituting a source of new cells. They produce neurons and glial cells in lower vertebrates but they mainly generate glial cells in mammals. The mechanisms underlying their activation and their glial-biased differentiation in mammals remain ill-defined. This represents an obstacle to control these cells. We addressed this issue using RNA profiling of ependymal cells before and after injury. We found that these cells activate STAT3 and ERK/MAPK signaling during injury and downregulate cilia-associated genes and FOXJ1, a central transcription factor in ciliogenesis. Conversely, they upregulate 510 genes, six of them more than 20 fold, namely Crym, Ecm1, Ifi202b, Nupr1, Rbp1, Thbs2 and Osmr. OSMR is the receptor for the inflammatory cytokine oncostatin (OSM) and we studied its regulation and role using neurospheres derived from ependymal cells. We found that OSM induces strong OSMR and p-STAT3 expression together with proliferation reduction and astrocytic differentiation. Conversely, production of oligodendrocyte-lineage OLIG1+ cells was reduced. OSM is specifically expressed by microglial cells and was strongly upregulated after injury. We observed microglial cells apposed to ependymal cells in vivo and co-cultures experiments showed that these cells upregulate OSMR in neurosphere cells. Collectively, these results support the notion that microglial cells and OSMR/OSM pathway regulate ependymal cells in injury. In addition, the generated high throughput data provides a unique molecular resource to study how ependymal cell react to spinal cord lesion.

The distribution of non-synaptic intercellular junctions during neurone differentiation in the developing spinal cord of the clawed toad

Development ◽  
1975 ◽  
Vol 33 (2) ◽  
pp. 403-417
Author(s):  
Brian P. Hayes ◽  
Alan Roberts
Keyword(s):  
Spinal Cord ◽  
Gap Junctions ◽  
Neural Differentiation ◽  
Electrical Coupling ◽  
Intercellular Junctions ◽  
Ependymal Cells ◽  
Freedom Of Movement ◽  
Ventricular Cells ◽  
Vertebrate Embryos ◽  
Developing Spinal Cord

The distribution of intercellular junctions, other than synapses and their precursors, has beendescribed in the developing spinal cord of Xenopus laevis between the neurula andfree swimming tadpole stages. At the neurocoel, ventricular cells are joined in the apical contactzone by a sequence of junctions which usually has one or more intermediate junctions but often also includes close appositions, gap junctions and desmosomes. This apical complex is more diverse than that reported in other vertebrate embryos and between ependymal cells in the adult central nervous system. Gap junctions are also found between ventricular cells and their processes near the external cord surface. However, no other special junctions occur in this location under the basementlamella which surrounds the cord. Punctate intermediate junctions are generally distributed between undifferentiated and differentiating cells and their processes but were not found in neuropil after stage 28. These results are discussed in relation to cell movements during neural differentiation, possible effects on the freedom of movement of ions and molecules through extracellular pathways in the embryo, and possible intercytoplasmic pathways via gap junctions which may be responsible for the physiologically observed electrical coupling between neural tube cells.

Grafting of Choroid Plexus Ependymal Cells Promotes the Growth of Regenerating Axons in the Dorsal Funiculus of Rat Spinal Cord: A Preliminary Report

2001 ◽  
Vol 167 (2) ◽  
pp. 242-251 ◽  
Author(s):  
Chizuka Ide ◽  
Masaaki Kitada ◽  
Shushovan Chakrabortty ◽  
Masanori Taketomi ◽  
Naoya Matsumoto ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Choroid Plexus ◽  
Preliminary Report ◽  
Ependymal Cells ◽  
Rat Spinal Cord ◽  
Dorsal Funiculus

scholarly journals Musashi and Plasticity of Xenopus and Axolotl Spinal Cord Ependymal Cells

2018 ◽  
Vol 12 ◽  
Author(s):  
Ellen A. G. Chernoff ◽  
Kazuna Sato ◽  
Hai V. N. Salfity ◽  
Deborah A. Sarria ◽  
Teri Belecky-Adams
Keyword(s):  
Spinal Cord ◽  
Ependymal Cells

scholarly journals Localized activation of ependymal progenitors induces EMT-mediated glial bridging after spinal cord injury

2020 ◽  
Author(s):  
Lili Zhou ◽  
Brooke Burris ◽  
Ryan Mcadow ◽  
Mayssa H. Mokalled
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Epithelial To Mesenchymal Transition ◽  
Ependymal Cells ◽  
Spinal Cord Tissue ◽  
Spinal Cord Regeneration ◽  
Enhancer Element ◽  
Mesenchymal Transition ◽  
Cord Injury ◽  
Spinal Cord Repair

ABSTRACTUnlike mammals, adult zebrafish undergo spontaneous recovery after major spinal cord injury. Whereas scarring presents a roadblock for mammalian spinal cord repair, glial cells in zebrafish form a bridge across severed spinal cord tissue to facilitate regeneration. Here, we performed FACS sorting and genome-wide profiling to determine the transcriptional identity of purified bridging glia. We found that Yap-Ctgf signaling activates epithelial to mesenchymal transition (EMT) in localized niches of ependymal cells to promote glial bridging and regeneration. Preferentially activated in early bridging glia, Yap is required for the expression of the glial bridging factor Ctgfa and for functional spinal cord repair. Ctgfa regulation is controlled by an injury responsive enhancer element that drives expression in early bridging glia after injury. Yap-Ctgf signaling activates a mesenchymal transcriptional program that drives glial bridging. This study revealed the molecular signatures of bridging glia and identified an injury responsive gene regulatory network that promotes spinal cord regeneration in zebrafish.

scholarly journals The Structure of the Spinal Cord Ependymal Region in Adult Humans Is a Distinctive Trait among Mammals

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2235
Author(s):  
Alejandro Torrillas de la Cal ◽  
Beatriz Paniagua-Torija ◽  
Angel Arevalo-Martin ◽  
Christopher Guy Faulkes ◽  
Antonio Jesús Jiménez ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Small Groups ◽  
Central Canal ◽  
Ependymal Cells ◽  
Injured Spinal Cord ◽  
Heterocephalus Glaber ◽  
Mole Rat ◽  
Naked Mole Rat ◽  
Adult Humans ◽  
Human Trait

In species that regenerate the injured spinal cord, the ependymal region is a source of new cells and a prominent coordinator of regeneration. In mammals, cells at the ependymal region proliferate in normal conditions and react after injury, but in humans, the central canal is lost in the majority of individuals from early childhood. It is replaced by a structure that does not proliferate after damage and is formed by large accumulations of ependymal cells, strong astrogliosis and perivascular pseudo-rosettes. We inform here of two additional mammals that lose the central canal during their lifetime: the Naked Mole-Rat (NMR, Heterocephalus glaber) and the mutant hyh (hydrocephalus with hop gait) mice. The morphological study of their spinal cords shows that the tissue substituting the central canal is not similar to that found in humans. In both NMR and hyh mice, the central canal is replaced by tissue reminiscent of normal lamina X and may include small groups of ependymal cells in the midline, partially resembling specific domains of the former canal. However, no features of the adult human ependymal remnant are found, suggesting that this structure is a specific human trait. In order to shed some more light on the mechanism of human central canal closure, we provide new data suggesting that canal patency is lost by delamination of the ependymal epithelium, in a process that includes apical polarity loss and the expression of signaling mediators involved in epithelial to mesenchymal transitions.

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