Inhibiting thrombin activity could treat PVR

August 8, 2014

Inhibiting thrombin activity may be a treatment option for proliferative vitreoretinopathy (PVR), given that such activity is increased in the vitreous of patients with the disease and is associated with the activation of pro-inflammatory and pro-fibrotic pathways in retinal pigment epithelium (RPE) cells.

Inhibiting thrombin activity may be a treatment option for proliferative vitreoretinopathy (PVR), given that such activity is increased in the vitreous of patients with the disease and is associated with the activation of pro-inflammatory and pro-fibrotic pathways in retinal pigment epithelium (RPE) cells. So say authors of a study published in Investigative Ophthalmology & Visual Science.

The authors, from The Netherlands, collected vitreous samples from 11 patients undergoing vitrectomy for macular holes and puckers, who served as controls; 15 patients with retinal detachment in whom PVR did not develop within 6 months after vitrectomy; 11 patients with retinal detachment in whom PVR did develop within 6 months after vitrectomy; and 14 patients with established PVR. They used a thrombin-specific chromogenic substrate to determine thrombin activity in the vitreous.

The researchers stimulated ARPE-19 cells with diluted vitreous samples with and without hirudin. They used a multiplex approach to analyse samples at 0 and 24 hours to see whether 27 cytokines/chemokines and growth factors were present.

Results showed that thrombin activity was significantly greater in the vitreous of the PVR group compared with the vitreous in the other groups. "PVR vitreous stimulated the production CCL2, CXCL8, GM-CSF, IL-6 and PDGF-BB by ARPE-19 to significantly (P

To read the abstract of the study, click here.