Abstract

Abstract Purpose Mohan et al, (2003) hypothesised that after corneal injury, the site of injury is invaded by myofibroblasts (MFBCs) derived from dividing keratocytes. We report here the distribution of myofibroblasts (MFBCs), and cellular location of α‐‐ smooth muscle actin (α‐‐SMA) in scarred cornea. Methods Three penetrating keratoplasty buttons, two with post‐zoster scarring and one with hypertrophic dendriform epitheliopathy, were fixed in: 1) 2.5% glutaraldehyde containing cuprolinic blue for ultrastructural studies and 2) 4% paraformaldehyde for immunogold localisation. Primary α‐‐SMA and vimentin antibodies were localised by gold conjugates. Results Large numbers of MFBCs were observed in the sub‐epithelial collagenous pannus, posterior stroma and posterior collagenous layer in these corneas. The MFBCs were very large in size, lay in layers and occasionally fused with each other. Labelling for α‐SMA was very strong in all MFBCs. Labelling of α‐SMA was also observed in basal epithelial cells. MFBCs contained very prominent rough endoplasmic reticulum, vimentin filaments and large nuclei. Significantly, large proteoglycans (nm) and collagen fibrils (nm) were present around these cells. Conclusion It has been suggested that cytokynes released from the overlying epithelium act to maintain the myofibroblast phenotype (Jester et al 1999a, 1999b). We hypothesise that MFBCs synthesise large amounts of proteoglycan which disrupt the organisation of collagen fibrils and lead to the opacities of scarred cornea. The finding of labelling for α‐SMA in basal epithelial cells suggests that some epithelial cells may transform into MFBCs.

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