A novel recombinant human microplasminogen induced complete posterior vitreous detachment without morphological change of retina in juvenile rabbits

Vitreomacular traction syndrome results from persistent vitreoretinal adhesions in the setting of partial posterior vitreous detachment (PVD). Vitrectomy and reattachment of retina is an effective therapeutic approach. The adhesion between vitreous cortex and internal limiting membrane (ILM) of the retina is stronger in youth, which brings difficulties to induce PVD in vitrectomy. Several clinical investigations demonstrated that intravitreous injection of plasmin before vitrectomy could reduce the risk of detachment. In our study, a novel recombinant human microplasminogen (rh mu Plg) was expressed by Pichia pastoris. Molecular docking showed that the binding of rh mu Plg with tissue plasminogen activator (t-PA) was similar to plasminogen, suggesting rh mu Plg could be activated by t-PA to generate microplasmin (mu Plm). Moreover, rh mu Plg had higher catalytic activity than plasminogen in amidolytic assays. Complete PVD was found at vitreous posterior pole of 125 mu g rh mu Plg-treated eyes without morphological change of retina in juvenile rabbits via intraocular injection. Our results demonstrate that rh mu Plg has a potential value in the treatment of vitreoretinopathy.

Automated summary

Vitreomacular traction syndrome is caused by persistent adhesion between the vitreous cortex and retinal internal limiting membrane. Vitrectomy and reattachment of retina are effective therapeutic approaches. Clinical investigations have shown that preoperative intravitreous plasmin injection reduces the risk of detachment. In this study, a novel recombinant human microplasminogen (rh mu Plg) was developed and shown to have potential value in the treatment of vitreoretinopathy.