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Updated: Apr 23, 2026

Isolation of Primary Murine Brain Microvascular Endothelial Cells
Published on: November 14, 2014
Brain endothelial cell specific integrins and ischemic stroke
Kathleen Guell1, Gregory J Bix
1Department of Anatomy and Neurobiology, University of Kentucky, Sanders Brown Building 800 South Limestone, Lexington, Kentucky 40508, USA.
Ischemic stroke, a devastating event caused by the blockage of a blood vessel(s) supplying the brain, continues to affect thousands of people in the USA every year. While no true advances in stroke therapy have arisen to further improve patient outcomes since the introduction of the blood clot buster tissue plasminogen activator and mechanical clot removal, fewer people are dying from the immediate stroke insult. Instead, patients often suffer significant morbidity due to post-recanalization secondary damage. Central to this damage is the breakdown of the blood-brain barrier, which, in addition to contributing to edema and inflammation, triggers an upregulation in angiogenic growth factors in the brain's attempt to salvage and repair itself. Recent studies have begun to improve our understanding of the post-stroke angiogenic response of brain endothelial cells in the ischemic penumbra, which has long been held to be an important site for medical intervention. These studies suggest that endothelial cell integrin matrix receptors play an important and therapeutically significant role in moderating cellular responses to ischemic brain injury.
Ischemic stroke, a devastating event caused by the blockage of a blood vessel(s) supplying the brain, continues to affect thousands of people in the USA every year. While no true advances in stroke therapy have arisen to further improve patient outcomes since the introduction of the blood clot buster tissue plasminogen activator and mechanical clot removal, fewer people are dying from the immediate stroke insult. Instead, patients often suffer significant morbidity due to post-recanalization secondary damage. Central to this damage is the breakdown of the blood-brain barrier, which, in addition to contributing to edema and inflammation, triggers an upregulation in angiogenic growth factors in the brain's attempt to salvage and repair itself. Recent studies have begun to improve our understanding of the post-stroke angiogenic response of brain endothelial cells in the ischemic penumbra, which has long been held to be an important site for medical intervention. These studies suggest that endothelial cell integrin matrix receptors play an important and therapeutically significant role in moderating cellular responses to ischemic brain injury.
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In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...

