Ischemia/Stroke
Stroke is a leading cause of morbidity and mortality worldwide, the most common form of which is ischemic stroke, caused by a blockage of blood flow to a specific part of the brain. Treatments for ischemic stroke include clot removal and prevention of clot reformation, but there is a lack of pharmaceuticals to prevent secondary injury from occurring and to promote regeneration. Despite decades of research, hundreds of therapies have failed to translate to patients. There is a need for new and complimentary models of stroke.
Currently we are developing an in vitro model of ischemic stroke using our rodent 3D neural microtissues. To replicate the blood supply disruption seen in stroke, cortical spheroids are subjected to oxygen-glucose deprivation (OGD) for 24 hours. We are exploring the effects of OGD on cell viability, morphology, and function with hopes to discover potential treatment targets for this devastating injury.
Capillary-like networks of laminin (red) are disrupted by oxygen and oxygen-glucose deprivation (OD and OGD), whereas controls and glucose deprived (GD) spheroids are able to maintain these networks.
Beta-iii-tubulin, a neural cytoskeletal marker, showed loss of strand-like structure and an increase in puncta after OGD.
Astrocytes in cortical spheroids subjected to OGD showed increased cell soma width and enhanced GFAP (glial fibrillary acid protein) expression as compared to controls.