No abstract

In sickle cell disease, deoxygenation of intra-erythrocytic hemoglobin S leads to hemoglobin polymerization, erythrocyte rigidity, hemolysis, and microvascular occlusion. Ischemia-reperfusion injury, plasma hemoglobin-mediated nitric oxide consumption, and free radical generation activate systemic inflammatory responses. To characterize the role of circulating leukocytes in sickle cell pathogenesis we performed global transcriptional analysis of blood mononuclear cells from 27 patients in steady-state sickle cell disease (

Copolymerization of nonmuscle myosins IIA and IIB followed by their differential turnover in stress fibers leads to self-sorting of IIA and IIB along the front–rear axis of the cell, thus producing a polarized actin cytoskeleton.