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The postoperative scarring response following glaucoma filtration remains the major cause of surgical failure. Priglinger et al. (930) investigated the role of a specific enzyme, tissue tranglutaminase (tTGase) on the development of scar tissue formation. One of the key functions of tTGase is to cross link extracellular matrix proteins such as fibronectin and collagen III through e(g-glutamyl)-lysine bonds, rendering them resistant to proteolytic degradation. In a series of elegant experiments, the authors demonstrated the colocalisation of tTGase mRNA and protein expression with fibronectin in failed blebs obtained from patients undergoing trabeculectomy revision. Immunohistochemical staining was most profound at the border of the Tenon cyst, which is where the site of the 'ring of steel' is reported. Expression of tTGase was significantly upregulated in the presence of TGF-b2 in cell cultures of human Tenon's fibroblasts and in an in vitro model of glaucoma filtration surgery. TGF-b2 is the most potent stimulator of ocular scarring, and this study demonstrated that TGF-b2 both increased tTGase expression in cultured HTF (human Tenon's fibroblasts) and enhanced crosslinking of fibronectin via the formation of e(g-glutamyl)-lysine bonds. Extracellular tTGase activity was also shown to be increased when the HTFs were pretreated with TGF-b2 in vitro. The in vitro model of trabeculectomy is the main weakness in the study. The major concern is that there is an absence of a blood supply which would have a significant impact on the experimental findings. Despite this however, the results of the paper clearly demonstrate that tTGase activity plays an important role in wound healing events following trabeculectomy.