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Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
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Related Experiment Video

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Dabigatran inhibits intravitreal thrombin activity.

Jeroen Bastiaans1, Verena C Mulder2, Jan C van Meurs2,3

  • 1Departments of Immunology, Erasmus MC, Rotterdam, The Netherlands.

Acta Ophthalmologica
|December 2, 2017
PubMed
Summary

Dabigatran, a direct thrombin inhibitor, effectively reduced pro-fibrotic and pro-inflammatory markers in retinal pigment epithelial cells. Oral dabigatran intake also inhibited thrombin activity in vitreous fluid, suggesting a potential therapeutic strategy for proliferative vitreoretinopathy.

Keywords:
dabigatranfibrosisinflammationproliferative vitreoretinopathyretinal pigment epitheliumthrombinvitreous

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Area of Science:

  • Ophthalmology
  • Vitreoretinal Diseases
  • Pharmacology

Background:

  • Proliferative vitreoretinopathy (PVR) involves retinal pigment epithelial (RPE) cell activation, leading to fibrotic membranes and inflammation.
  • Elevated intravitreal thrombin activity in PVR patients promotes profibrotic and proinflammatory RPE cell responses.

Purpose of the Study:

  • To investigate the efficacy of dabigatran, a direct thrombin inhibitor, in mitigating thrombin-induced RPE cell activation.
  • To assess the potential of dabigatran as a therapeutic agent for PVR by inhibiting intravitreal thrombin activity.

Main Methods:

  • ARPE-19 cells were exposed to thrombin or vitreous fluid (with or without elevated thrombin activity) in the presence or absence of dabigatran.
  • Gene expression of inflammatory markers (CCL2, CXCL8, GMCSF, IL6, PDGFB) and protein levels of 27 cytokines/chemokines/growth factors were analyzed.
  • In vitro thrombin activity assays were performed on vitreous fluid from patients after oral dabigatran intake.

Main Results:

  • Thrombin and PVR vitreous fluid induced expression of CCL2, CXCL8, GM-CSF, IL-6, and PDGF-BB in RPE cells.
  • Dabigatran significantly inhibited these thrombin-induced gene expressions.
  • Vitreous fluid from patients on oral dabigatran showed reduced thrombin activity in vitro.

Conclusions:

  • Intravitreal thrombin activity drives profibrotic and proinflammatory pathways in RPE cells, contributing to PVR.
  • Dabigatran demonstrates potential to inhibit these pathological pathways, offering a promising therapeutic avenue for PVR.