Just in rats so YOU will need to ask your doctor what research group they are collaborating with to test this in humans. No collaboration, call the hospital president and demand the incompetent stroke department head be fired. Someone has to light a fire under our stroke medical 'professionals' since they aren't doing it themselves.
Yes, I am a bad person, wanting some competency in stroke recovery.
MicroRNA cluster miR-17–92 Cluster in Exosomes Enhance Neuroplasticity and Functional Recovery After Stroke in Rats
Abstract
Background and Purpose—Multipotent
mesenchymal stromal cell (MSC) harvested exosomes are hypothesized as
the major paracrine effectors of MSCs. In vitro, the miR-17–92 cluster
promotes oligodendrogenesis, neurogenesis, and axonal outgrowth. We,
therefore, investigated whether the miR-17–92 cluster–enriched exosomes
harvested from MSCs transfected with an miR-17–92 cluster plasmid
enhance neurological recovery compared with control MSC-derived
exosomes.
Methods—Rats
subjected to 2 hours of transient middle cerebral artery occlusion were
intravenously administered miR-17–92 cluster–enriched exosomes, control
MSC exosomes, or liposomes and were euthanized 28 days post–middle
cerebral artery occlusion. Histochemistry, immunohistochemistry, and
Golgi–Cox staining were used to assess dendritic, axonal, synaptic, and
myelin remodeling. Expression of phosphatase and tensin homolog and
activation of its downstream proteins, protein kinase B, mechanistic
target of rapamycin, and glycogen synthase kinase 3β in the peri-infarct
region were measured by means of Western blots.
Results—Compared
with the liposome treatment, both exosome treatment groups exhibited
significant improvement of functional recovery, but miR-17–92
cluster–enriched exosome treatment had significantly more robust effects
on improvement of neurological function and enhancements of
oligodendrogenesis, neurogenesis, and neurite remodeling/neuronal
dendrite plasticity in the ischemic boundary zone (IBZ) than the control
MSC exosome treatment. Moreover, miR-17–92 cluster–enriched exosome
treatment substantially inhibited phosphatase and tensin homolog, a
validated miR-17–92 cluster target gene, and subsequently increased the
phosphorylation of phosphatase and tensin homolog downstream proteins,
protein kinase B, mechanistic target of rapamycin, and glycogen synthase
kinase 3β compared with control MSC exosome treatment.
Conclusions—Our
data suggest that treatment of stroke with tailored exosomes enriched
with the miR-17–92 cluster increases neural plasticity and functional
recovery after stroke, possibly via targeting phosphatase and tensin
homolog to activate the PI3K/protein kinase B/mechanistic target of
rapamycin/glycogen synthase kinase 3β signaling pathway.
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