Background and Purpose— Apposition of endothelial cells and astrocyte foot processes to the basal lamina matrix is postulated to underlie the cerebral microvessel permeability barrier. Focal cerebral ischemia induces rapid loss of select matrix-binding integrins from both cell compartments in the nonhuman primate. This study is the first to examine the conditions underlying integrin loss from these cell-types during ischemia in vitro and their relation to the changes in vivo.

Methods— The impact of normoxia or standardized oxygen-glucose deprivation on integrin expression by murine primary cerebral endothelial cells and astrocytes grown on matrix substrates (collagen IV, laminin, and perlecan) of the basal lamina were quantitatively assessed by flow cytometry.

Results— Endothelial cell expression of the β1 and α5 subunits significantly increased on all matrix ligands, whereas astrocytes displayed modest significant decreases in α5 and α6 subunits. Oxygen-glucose deprivation produced a further significant increase in subunit β1 expression by both cell types, but a clear decrease in both α1 and α6 subunits by murine astrocytes.

Conclusions— Ischemia in vitro significantly increased endothelial cell β1 expression, which is consistent with the increase in β1 transcription by microvessels peripheral to the ischemic core. The loss of α1 and α6 integrins from murine astrocytes is identical to that seen in the nonhuman primate in vivo. These findings establish both isolated murine cerebral endothelial cells and astrocytes as potential integrin response cognates of microvascular cells of the neurovascular unit in primates, and allow determination of the mechanisms of their changes to ischemia.