Why the study?
The formation of vascular tubes is driven by extensive changes in endothelial cell shape, but the underlying molecular mechanisms modulating the mechanical properties of the endothelial cell cortex remained to be clarified.
Marcksl1 regulates the mechanical properties of the endothelial cell cortex by balancing linear and branched actin networks to resist blood flow forces and control vessel structure.
Marcksl1 modulation of endothelial mechanics is hypothesis-generating for angiogenesis; leaves open therapeutic translation pending human validation.
The formation of vascular tubes is driven by extensive changes in endothelial cell (EC) shape. Here, we have identified a role of the actin-binding protein, Marcksl1, in modulating the mechanical properties of EC cortex to regulate cell shape and vessel structure during angiogenesis. Increasing and depleting Marcksl1 expression level in vivo results in an increase and decrease, respectively, in EC size and the diameter of microvessels. Furthermore, endothelial overexpression of Marcksl1 induces ectopic blebbing on both apical and basal membranes, during and after lumen formation, that is suppressed by reduced blood flow. High resolution imaging reveals that Marcksl1 promotes the formation of linear actin bundles and decreases actin density at the EC cortex. Our findings demonstrate that a balanced network of linear and branched actin at the EC cortex is essential in conferring cortical integrity to resist the deforming forces of blood flow to regulate vessel structure.
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Kondrychyn et al. (2020) studied this question.
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