Thursday, June 19, 2014
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Tumor necrosis factor receptor superfamily member
activator of NF-kB ligand
In vitro and mouse studies suggest RANKL could help reduce
ischemic brain damage following stroke. OPG, which binds RANKL and inhibits
signaling through RANK
is upregulated following stroke. In mice, Opg knockout or
intracerebroventricular injection of Rankl decreased infarct volume and
cerebral edema following middle cerebral artery occlusion compared with no
knockout or injection of a control protein. In the mice with cerebral artery
occlusion, a Rankl-neutralizing antibody increased infarct volume compared
with a control protein. In neurons cocultured with microglia, RANKL inhibited
inflammatory cytokines and neuronal cell death. Next steps include assessing
the effects of systemic RANKL delivery on ischemic injury.
Published online June 19, 2014
Patent application filed;
available for licensing
Shimamura, M. et al.
Proc. Natl. Acad. Sci. USA; published online May 20, 2014;
Contact: Ryuichi Morishita, United Graduate School of Child
Development, Osaka, Japan
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