Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Tuesday, February 28, 2017

MicroRNA cluster miR-17–92 Cluster in Exosomes Enhance Neuroplasticity and Functional Recovery After Stroke in Rats

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.
http://stroke.ahajournals.org/content/early/2017/02/23/STROKEAHA.116.015204
Hongqi Xin, Mark Katakowski, Fengjie Wang, Jian-Yong Qian, Xian Shuang Liu, Meser M. Ali, Benjamin Buller, Zheng Gang Zhang, Michael Chopp

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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