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The Journal of Neuroscience, October 26, 2005, 25(43):9940-9948; doi:10.1523/JNEUROSCI.3467-05.2005

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Development/Plasticity/Repair
Vascular Development of the Brain Requires 8 Integrin Expression in the Neuroepithelium

John M. Proctor,¹ Keling Zang,¹ Denan Wang,¹ Rong Wang,² and Louis F. Reichardt¹

¹Howard Hughes Medical Institute and Department of Physiology, and ²Department of Surgery, University of California, San Francisco, California 94143

We showed previously that loss of the integrin 8 subunit, which forms v8 heterodimers, results in abnormal vascular development in the yolk sac, placenta, and brain. Animals lacking the integrin 8 (itg8) gene die either at midgestation, because of insufficient vascularization of the placenta and yolk sac, or shortly after birth with severe intracerebral hemorrhage. To specifically focus on the role of integrins containing the 8 subunit in the brain, and to avoid early lethalities, we used a targeted deletion strategy to delete itg8 only from cell types within the brain. Ablating itg8 from vascular endothelial cells or from migrating neurons did not result in cerebral hemorrhage. Targeted deletion of itg8 from the neuroepithelium, however, resulted in bilateral hemorrhage at postnatal day 0, although the phenotype was less severe than in itg8-null animals. Newborn mice lacking itg8 from the neuroepithelium had hemorrhages in the cortex, ganglionic eminence, and thalamus, as well as abnormal vascular morphogenesis, and disorganized glia. Interestingly, adult mice lacking itg8 from cells derived from the neuroepithelium did not show signs of hemorrhage. We propose that defective association between vascular endothelial cells and glia lacking itg8 is responsible for the leaky vasculature seen during development but that an unidentified compensatory mechanism repairs the vasculature after birth.

Key words: brain; cortex; hemorrhage; integrin; neuroepithelium; vasculature

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Received Jan 7, 2005; revised September 9, 2005; accepted September 11, 2005.

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