Abstract
Cerebral cavernous malformation (CCM) proteins play critical roles for endothelial cell functions, including cytoskeletal remodeling, cell-cell interactions, cell polarity, tube formation, and angiogenesis. It has been shown that the mutation of even one of the CCM genes involved in CCMs can determine an alteration in the angiogenesis process, but the precise mechanism is yet to be clarified.Here using a model of cerebral microvascular endothelial cells (hBMEC) transiently silenced by CCM1, we tried to mimic the physiological conditions that occur in the presence of CCM1 gene know-down evaluating their ability to form tube structures through an in vitro angiogenesis assay.
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