Exogenous fractalkine enhances proliferation of endothelial cells, promotes migration of endothelial progenitor cells and improves neurological deficits in a rat model of ischemic stroke.

Fractalkine/CX3CL1, also called neurotactin, has been described as an angiogenic agent, and its expression is up-regulated in the penumbra after ischemia. This study was conducted to investigate the neovascular potential of fractalkine on rat models of transient middle cerebral artery occlusion (MCAO). Rats receiving intracerebroventricular injections of fractalkine were found to have improved neurological deficits, reduced cerebral infarct size and increased neuron survival for both doses (100ng and 1μg). Fractalkine exerted angiogenic effects that showed dose-dependent higher vascular densities in the peri-infarct area. Furthermore, exogenous fractalkine increased the proliferation of endothelial cells in a dose-dependent manner and enhanced the migration of endothelial progenitor cells at the higher dose (1μg) in ischemic penumbra. In conclusion, intracerebroventricular administration of fractalkine reduces ischemic damage by promoting neuroprotection and by inducing endothelial cell proliferation and endothelial progenitor cell migration, thereby enhancing neovascularization in the peri-infarct region.