The Structure of the Spinal Cord Ependymal Region in Adult Humans Is a Distinctive Trait among Mammals.
Alejandro Torrillas de la CalBeatriz Paniagua-TorijaAngel Arevalo-MartinChristopher Guy FaulkesAntonio Jesús JiménezIsidro FerrerEduardo Molina-HolgadoDaniel Garcia-OvejeroPublished in: Cells (2021)
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.
Keyphrases
- induced apoptosis
- spinal cord
- cell cycle arrest
- endothelial cells
- stem cells
- oxidative stress
- magnetic resonance
- cell death
- endoplasmic reticulum stress
- type diabetes
- high resolution
- neuropathic pain
- signaling pathway
- genome wide
- metabolic syndrome
- machine learning
- adipose tissue
- deep learning
- subarachnoid hemorrhage
- brain injury
- wild type
- cell proliferation
- mass spectrometry