Figure 1: The shape of the apical surface of the corneal endothelial cells (CECs) depends on the actomyosin network and tight-junctions.

(A) Myosin IIa and actin colocalized and formed a network just beneath the apical cell membrane. (Confocal microscopy, central cornea from a 16 years old patient with normal CECs and keratoconus) (B) The myosin network was perfectly aligned and connected with tight junctions, here highlighted by one of its components, ZO-1 (Epifluorescence microscopy, central cornea of a 68 years old patient with normal CECs and stromal hereditary dystrophy). (C) Illustration of the contractility of the actomyosin network in 3 situations. In normal CECs, forces between cells were balanced and responsible for straight borders. In the case of spontaneous isolated death, neighbor cells presented only one retracted border. The lateral cytoplasmic expansions became clearly visible in the area left empty by the dead cell. After treatment with ethylenediaminetetraacetic acid, which disrupted tight junctions, contraction of the network rounded the apical surface while leaving the lateral expansions almost intact. (Pair of corneas of a 66 years old donor with normal CECs).