Caco-2 cells labeled for tight junction molecule cingulin (green), actin (red), vinculin (pink) and DNA (blue).
Epithelial cells growing on a patterned adhesive surface with the shape of the Weizmann Institute tree.
Desmosomes in mouse tongue epithelium (by transmission electron microscope).
Porcine aortic endothelial cell, double-labeled for actin (green) and phospho-tyrosine (red).
“Molecular composition map” of focal adhesions and stress fibers.
Myeloma cancer cell responding to shear flow (by scanning electron microscope).
Platelet adhesion
Platelets are megakaryocyte-derived fragments that play a major role in regulating hemostasis. Upon rupture of blood vessels, they adhere to the ECM around the wound edge, aggregate locally, and suppress the bleeding. The adhesion and activation processes are integrin-dependent, and are accompanied by radical changes in the organization of the cytoskeleton. Preliminary studies demonstrated that this dramatic reorganization involves multiple adhesion proteins, clearly distinct from those found in focal adhesions of such cells as fibroblasts, epithelia and endothelia (Figure 1).
Figure 1
Platelet Adhesion. Platelets cultured for 2 hrs, fixed and labeled for vinculin (red) and actin (green).
We investigate these unique adhesions to fibrinogen, fibronectin, or collagen, using conventional and super-resolution fluorescence microscopy, and combine it with cryoelectron tomography (in collaboration with Prof. Ohad Medalia).