Co-Authors:
McCarty, J.H., M.I.T. E17-230, Cambridge, MA 02139, United States
Monahan-Earley, R.A., M.I.T. E17-230, Cambridge, MA 02139, United States
Brown, L.F., M.I.T. E17-230, Cambridge, MA 02139, United States
Keller, M., M.I.T. E17-230, Cambridge, MA 02139, United States
Gerhard, H., M.I.T. E17-230, Cambridge, MA 02139, United States
Rubin, K., M.I.T. E17-230, Cambridge, MA 02139, United States
Shani, M., M.I.T. E17-230, Cambridge, MA 02139, United States
Dvorak, H.F., M.I.T. E17-230, Cambridge, MA 02139, United States
Wolburg, H., M.I.T. E17-230, Cambridge, MA 02139, United States
Bader, B.L., M.I.T. E17-230, Cambridge, MA 02139, United States
Dvorak, A.M., M.I.T. E17-230, Cambridge, MA 02139, United States
Hynes, R.O., M.I.T. E17-230, Cambridge, MA 02139, United States
Abstract:
Mouse embryos genetically null for the αv integrin subunit develop intracerebral hemorrhages at midgestation and die shortly after birth. A key question is whether the hemorrhage arises from primary defects in vascular endothelial cells or pericytes or from other causes. We have previously reported normal initiation of cerebral vessels comprising branched tubes of endothelial cells. Here we show that the onset of hemorrhage is not due to defects in pericyte recruitment. Additionally, most αv-null vessels display ultrastructurally normal endothelium-pericyte associations and normal interendothelial cell junctions. Thus, endothelial cells and pericytes appear to establish their normal relationships in cerebral microvessels. However, by both light and electron microscopy, we detected defective associations between cerebral microvessels and the surrounding brain parenchyma, composed of neuroepithelial cells, glia, and neuronal precursors. These data suggest a novel role for αv integrins in the association between cerebral microvessels and central nervous system parenchymal cells.
תפריט נגישות
ניגודיות עדינה
מונוכרום
הדגשת קישורים
חסימת אנימציה
פונט קריא
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איפוס הגדרות נגישות
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