Deans' stroke musings: Vascular Stat3 Promotes Angiogenesis and Neuroplasticity Long-Term After Stroke

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, March 24, 2015

Vascular Stat3 Promotes Angiogenesis and Neuroplasticity Long-Term After Stroke

Everything this does would be incredibly helpful to our recovery. So when is your stroke department following up and creating a stroke protocol from this? 50 years from now? What does your hospital president have to say about the lack of competence in their stroke department?
http://circ.ahajournals.org/content/early/2015/03/20/CIRCULATIONAHA.114.013003.abstract

+ Author Affiliations

¹Charité-Universitätsmedizin Berlin, Germany
²Max-Delbrück Center for Molecular Medicine, Berlin, Germany
³Institute of Clinical Neurobiology, University Hospital, University of Würzburg, Germany
⁴Max-Delbrück Center for Molecular Medicine, Berlin, Germany & Cluster of Excellence NeuroCure, Charité-Universitätsmedizin Berlin, Germany
⁵Charité-Universitätsmedizin Berlin, Germany; German Center for Neurodegenerative Diseases (DZNE), Partner Site, Berlin, Germany; German Center for Cardiovascular Diseases (DZHK), Partner Site, Berlin, Germany

↵* Center for Stroke Research, Charité-University Medicine Berlin, Robert-Koch Platz 4, D-10115 Berlin, Germany christoph.harms@charite.de

Abstract

Background—Post-stroke angiogenesis contributes to long-term recovery after stroke. Signal transducer and activator of transcription-3 (Stat3) is a key regulator for various inflammatory signals and angiogenesis. It was the aim of this study to determine its function in post stroke outcome.

Methods and Results—We generated a tamoxifen-inducible and endothelial-specific Stat3 knockout mouse model by crossbreeding Stat3^floxed/KO and Tie2-Cre^ERT2 mice. Cerebral ischemia was induced by 30 minutes of middle cerebral artery occlusion (MCAo). We demonstrated that endothelial Stat3 ablation did not alter lesion size 2 days after ischemia but did worsen functional outcome at 14 days and increase lesion size at 28 days. At this late time point vascular Stat3 expression and phosphorylation were still increased in wildtype mice. Gene array analysis of a CD31-enriched cell population of the neurovascular niche showed that endothelial Stat3 ablation led to a shift toward an anti-angiogenic and axon growth-inhibiting micro-milieu after stroke, with an increased expression of Adamts9. Remodeling and glycosylation of the extracellular matrix (ECM) as well as microglia proliferation were increased while angiogenesis was reduced.

Conclusions—Endothelial Stat3 regulates angiogenesis, axon growth and ECM-remodeling and is essential for long-term recovery after stroke. It might serve as a potent target for stroke treatment after the acute phase by fostering angiogenesis and neuroregeneration.