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Cardiovascular disease

Ischemia/reperfusion injury

Tumor necrosis factor receptor superfamily member 11b (TNFRS11B; OPG); receptor activator of NF-kB ligand (RANKL; TNFSF11)

In vitro and mouse studies suggest RANKL could help reduce ischemic brain damage following stroke. OPG, which binds RANKL and inhibits signaling through RANK (TNFRSF11A; CD265), 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 lipopolysaccharide (LPS)-induced inflammatory cytokines and neuronal cell death. Next steps include assessing the effects of systemic RANKL delivery on ischemic injury.

SciBX 7(24); doi:10.1038/scibx.2014.708
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