Deans' stroke musings: Kruppel-like Factor 2 Protects Against Ischemic Stroke by Regulating Endothelial Blood Brain Barrier Function

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, January 22, 2013

Kruppel-like Factor 2 Protects Against Ischemic Stroke by Regulating Endothelial Blood Brain Barrier Function

This sounds like another cascade of death cause needing amelioration. Your researcher needs to work on this also.
http://ajpheart.physiology.org/content/early/2013/01/14/ajpheart.00712.2012.abstract

Abstract

During an ischemic stroke normal brain endothelial function is perturbed resulting in blood brain barrier (BBB) breakdown with subsequent infiltration of activated inflammatory blood cells, ultimately leading to neuronal cell death. Kruppel-like factor 2 (KLF2) is regulated by flow, is highly expressed in vascular endothelial cells (ECs), and serves as a key molecular switch regulating endothelial function and promoting vascular health. In this study we sought to determine the role of KLF2 in cerebrovascular function and the pathogenesis of ischemic stroke. Transient middle cerebral artery occlusion (tMCAO) was performed in KLF2 deficient (KLF2^-/-), KLF2 overexpressing (KLF2^tg), and control mice and stroke volume analyzed. BBB function was assessed in vivo by real time neuroimaging using positron emission tomography (PET) and Evan's blue dye (EBD) assay. KLF2^-/- mice exhibited significantly larger strokes and impairment in BBB function. In contrast, KLF2^tg mice were protected against ischemic stroke and demonstrated preserved BBB function. In concordance, gain and loss of function studies in primary brain microvascular ECs using transwell assays revealed KLF2 to be BBB protective. Mechanistically, KLF2 was demonstrated, both in vitro and in vivo, to regulate the critical BBB tight junction factor occludin. These data are first to identify endothelial KLF2 as a key regulator of the BBB and a novel neuroprotective factor in ischemic stroke.