OASIS deletion did not inhibit astrocyte migration but reduced the excessive accumulation of N-cadherin-expressing reactive astrocytes that formed the glial scar around the injury site.
A stab wound was introduced in the cerebellum of the L1/GAP-43 transgenic mice and a lentiviral vector (LV) carrying the polysialyltransferase (PST) cDNA (LV/PST) was injected into the lesion site to transduce the cells in the glial scar.
And it could also decrease the expression of the glial scar marker glial fibrillary acidic protein (GFAP), neurocan and phosphacan in the peri-infarct region and markedly reduce the thickness of glial scar after ischemia/reperfusion (I/R).
And it could also decrease the expression of the glial scar marker glial fibrillary acidic protein (GFAP), neurocan and phosphacan in the peri-infarct region and markedly reduce the thickness of glial scar after ischemia/reperfusion (I/R).
And it could also decrease the expression of the glial scar marker glial fibrillary acidic protein (GFAP), neurocan and phosphacan in the peri-infarct region and markedly reduce the thickness of glial scar after ischemia/reperfusion (I/R).
At 14 d post-injury, 0.5 mg/kg rapamycin significantly reduced the area and thickness of glial scar and chondroitin sulfate proteoglycan expression, accompanied by decreased expression of p-S6 and enhanced expression of growth associated protein 43 (an axon regeneration marker) in the region of glial scar.
Further, hUCB induced upregulation of MMP-2 reduced formation of the glial scar at the site of injury along with reduced immunoreactivity to chondroitin sulfate proteoglycans.
Gain- and loss-of-function studies in primary astrocytes indicated that Egr-1 regulates the transcription of chondroitin sulfate proteoglycans genes, the main extracellular matrix proteins of the glial scar.
Hyperbaric oxygen reduced the inflammatory reaction and glial scar formation by inhibiting inflammation-related factors iNOS and COX-2 and glial scar-related components GFAP and NG2.
Hyperbaric oxygen reduced the inflammatory reaction and glial scar formation by inhibiting inflammation-related factors iNOS and COX-2 and glial scar-related components GFAP and NG2.
Hyperbaric oxygen reduced the inflammatory reaction and glial scar formation by inhibiting inflammation-related factors iNOS and COX-2 and glial scar-related components GFAP and NG2.
In addition, adjudin treatment after stroke promoted functional and neurovascular recovery accompanied with the decreased area of glial scar in WT mice, which was blunted by Sirt3 deficiency.