Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,372 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Friday, September 28, 2018
Astrocyte-Derived Exosomes Treated With a Semaphorin 3A Inhibitor Enhance Stroke Recovery via Prostaglandin D2 Synthase
Have your doctor and stroke hospital follow this up with the researchers they work with for human testing. Or are they going to be incompetent like usual and DO NOTHING?
Exosomes
play a pivotal role in neurogenesis. In the peri-infarct area after
stroke, axons begin to regenerate but are inhibited by astrocyte scar
formation. The direct effect and underlying molecular mechanisms of
astrocyte-derived exosomes on axonal outgrowth after ischemia are not
known.
Methods—
Using
a semaphorin 3A (Sema3A) inhibitor, we explored neuronal signaling
during axonal outgrowth after ischemia in rats subjected to middle
cerebral artery occlusion and in cultured cortical neurons challenged
with oxygen-glucose deprivation. Furthermore, we assessed whether this
inhibitor suppressed astrocyte activation and regulated
astrocyte-derived exosomes to enhance axonal outgrowth after ischemia.
Results—
In
rats subjected to middle cerebral artery occlusion, we administered a
Sema3A inhibitor into the peri-infarct area from 7 to 21 days after
occlusion. We found that phosphorylated high-molecular weight
neurofilament-immunoreactive axons were increased, glial fibrillary
acidic protein–immunoreactive astrocytes were decreased, and functional
recovery was promoted at 28 days after middle cerebral artery occlusion.
In cultured neurons, the Sema3A inhibitor decreased Rho family GTPase
1, increased R-Ras, which phosphorylates Akt and glycogen synthase
kinase 3β (GSK-3β), selectively increased phosphorylated GSK-3β in
axons, and thereby enhanced phosphorylated high-molecular weight
neurofilament-immunoreactive axons after oxygen-glucose deprivation. In
cultured astrocytes, the Sema3A inhibitor suppressed activation of
astrocytes induced by oxygen-glucose deprivation. Exosomes secreted from
ischemic astrocytes treated with the Sema3A inhibitor further promoted
axonal elongation and increased prostaglandin D2 synthase expression on microarray analysis. GSK-3β+ and prostaglandin D2 synthase+ neurons were robustly increased after treatment with the Sema3A inhibitor in the peri-infarct area.
Conclusions—
Neuronal
Rho family GTPase 1/R-Ras/Akt/GSK-3β signaling, axonal GSK-3β
expression, and astrocyte-derived exosomes with prostaglandin D2 synthase expression contribute to axonal outgrowth and functional recovery after stroke.
No comments:
Post a Comment