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Angiogenesis is the formation of new blood vessels from existing vasculature. During this formation, endothelial cells migrate towards an angiogenic cue. This thesis investigates the role of the actin cytoskeleton and the motor protein myosin in this angiogenic migration. Endothelial cells were seeded on flat gels (2D) mimicking the cell's natural environment. The cells were imaged using confocal microscopy. Cell tractions are then extracted using traction force microscopy, a technique based on measuring local displacements around the cell and then calculating tractions by combining the displacement field with the known stiffness of the gel. Over 200 cells were processed this way, serving as an in-house database of the pool of human endothelial cells used in the MAtrix group (Mechanobiology research group of Katholieke Universiteit Leuven(KUL)). The imaged cells were also subjected to chemical reactants for one hour. These acto-myosin modifiers affect specific parts of the cell's structural proteins. Calyculin A and blebbistatin increase and decrease myosin activity respectively. Cytochalasin D and jasplakinolide target the actin cytoskeleton. The given calyculin A concentration does not produce differences in cell traction behaviour, but onset of the cell rounding up was found in the morphological analysis. Blebbistatin significantly decreases cell traction behaviour while increasing protrusion-forming activity. Cytochalasin D prevents the formation of actin cytoskeleton structures, inhibiting the cell's ability to enact forces. Jasplakinolide induces mass depletion of free actin in the cell, breaking down the actin cytoskeleton. These results tell us more on the importance of actin and myosin in cell migration. The results mainly serve as a reference for 3D experiments using the same acto-myosin modifiers, which are ongoing in the MAtrix group.