Interactions between platelets, leukocytes, and activated endothelial cells are important during microvascular occlusion; however, the regulatory mechanisms of these heterotypic cell-cell interactions remain unclear. Here, using intravital microscopy to evaluate mice lacking specific isoforms of the serine/threonine kinase AKT and bone marrow chimeras, we found that hematopoietic cell–associated AKT2 is important for neutrophil adhesion and crawling and neutrophil-platelet interactions on activated endothelial cells during TNF-α–induced venular inflammation. Studies with an AKT2-specific inhibitor and cells isolated from WT and
Jing Li, Kyungho Kim, Eunsil Hahm, Robert Molokie, Nissim Hay, Victor R. Gordeuk, Xiaoping Du, Jaehyung Cho
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