The calcium-binding protein Mtsl/S100A4 in normal, degenerating and demyelinated spinal cord of the adult mouse
- VernacularTitle:The calcium-binding protein Mtsl/S100A4 in normal,degenerating and demyelinated spinal cord of the adult mouse
- Author:
Zhengyu FANG
;
Liang XIONG
;
Xiaolin HUANG
;
Ning ZHOU
;
Elena KOZLOVAALDSKOGIUS
- Publication Type:Journal Article
- Keywords:
calcium-binding protein;
degeneration;
demyelination;
Mtsl/S100A4
- From:
Chinese Journal of Rehabilitation Medicine
2008;23(8):678-682,插页1
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression pattern of Mtsl/S100A4 in mouse spinal cord;to investigate the effects of Mtsl/S100A4 on glial cell responses.Method:The study was carried out on Mtsl/S100A4 wild type and knock-out mice.The degenerative spinal cord model was established by dorsal root or sciatic nerve injury.The de-myelinated spinal cord model was established by ethidium bromide injections.Then the expressions of S100A4,GFA P,NG2 and Mael were measured.Result:The expressions of Mtsl/S100A4 in mice spinal cord were similar to that in rats.In WT mice this protein expressed in a thin layer of fiber bundles in the tract of Lissauer,and in white matter astrocytes.There was intracellular up-regulation of Mtsl/S100A4 in white matter astrocytes of WT mice after dorsal root or sciatic nerve injury,with no difference in glial cell response between WT and KO mice.However,7 days after ethidium bromide injection,in WT mice,the astroglial reaction was restricted on operated side,where a distinct glial scar had formed.While in KO mice,no distinct glial scar formed in demyelinated area.Conclusion:Mtsl/S100A4 expression in mouse spinal cord is similar to the pattern as in rats;intracellular Mtsl/ S100A4 up-regulation does not affect glial responses in degenerative spinal cord;the presence of extracellular Mtsl/ S100A4,which entered the spinal cord after ethidium bromide induced demyelination,markedly affects the glial cell responses in demyelinative spinal cord,including glial scar formation.
