Betacellulin enhances endogenous repair mechanisms after ischemic stroke.

Stroke is the third major cause of death and single disability in developed countries. Ischemic stroke represents the majority of total diagnosed cases. Nowadays the only treatment for ischemic stroke is the administration of tPA. Because of hemorrhagic transformation risk, tPA treatment can only be administered at the onset of the symptoms generating a lack of available treatment for the rest of the patients. In the adult brain, neurogenesis persists in germinal areas known as niches which are specific areas with a particular microenvironment. In niches, neurogenesis is regulated by signals from adjacent cells and the extracellular matrix. Betacellulin is a protein secreted by the endothelial cells close to the brain niche and is thought to contribute to homeostasis and endogenous repair after injury. When betacellulin is infused into the lateral ventricles of mice, it induces neurogenesis and increases cell proliferation in the SVZ. Here we propose betacellulin as a promising treatment for ischemic stroke. Stroke was induced in rats by middle cerebral artery occlusion and betacellulin was administered via osmotic pump for 14 days. Changes in cell populations in the brain niche and damaged areas were analyzed in order to determine regeneration. Results suggest that betacellulin enhances endogenous repair systems that could be useful for functional recovery after stroke.