June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
The Endothelin Receptor Antagonist Macitentan Acts through both Vascular and Cellular Mechanisms to Promote Neuroprotection of Retinal Ganglion Cells in Rodents.
Author Affiliations & Notes
  • Raghu R Krishnamoorthy
    Pharmacology and Neuroscience, NTERI, University of North Texas Health Science Center, Fort Worth, Texas, United States
  • Bindu Kodati
    Pharmacology and Neuroscience, NTERI, University of North Texas Health Science Center, Fort Worth, Texas, United States
  • Sai H Chavala
    CIRC Biosciences, Inc.,, Chicago, Illinois, United States
  • Wei Zhang
    Pharmacology and Neuroscience, NTERI, University of North Texas Health Science Center, Fort Worth, Texas, United States
  • Dorota Luiza Stankowska
    Pharmacology and Neuroscience, NTERI, University of North Texas Health Science Center, Fort Worth, Texas, United States
  • Footnotes
    Commercial Relationships   Raghu Krishnamoorthy None; Bindu Kodati None; Sai Chavala None; Wei Zhang None; Dorota Stankowska None
  • Footnotes
    Support  NIH Grant EY028179
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 1484. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Raghu R Krishnamoorthy, Bindu Kodati, Sai H Chavala, Wei Zhang, Dorota Luiza Stankowska; The Endothelin Receptor Antagonist Macitentan Acts through both Vascular and Cellular Mechanisms to Promote Neuroprotection of Retinal Ganglion Cells in Rodents.. Invest. Ophthalmol. Vis. Sci. 2022;63(7):1484.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose : The endothelin system has been shown to be a contributor to neurodegeneration in rodent models of glaucoma. The purpose of this study was to determine if the endothelin receptor antagonist, macitentan, could promote neuroprotection by blocking endothelin-1 (ET-1) mediated vasoconstrictive changes as well as reduce RGC loss and axonal injury during ocular hypertension.

Methods : Adult retired breeder male and female Brown Norway rats were either untreated or treated with macitentan (5 mg/kg body wt) in dietary gels three days per week. Following the treatments, the rats were intravitreally injected in one eye with 4 ml of 500 mM ET-1 and the retinal vasculature was imaged in a Micron IV retinal imaging system. In a parallel set of experiments IOP was elevated in one eye of Brown Norway rats and the animals were treated with macitentan for 4 weeks in dietary gels. Pattern ERG analysis, RGC counts and PPD staining of optic nerve sections were carried out.

Results : ET-1 administration produced rapid vasoconstrictive effects in retinal arteries that occurred 5 min after intravitreal administration and recovery began to occur 20 minutes post-injection. Rats treated with macitentan in the diet abrogated the ET-1 mediated vasoconstrictive effects or delayed its onset. Following IOP elevation in rats, untreated rats exhibited a significant 32% loss of RGCs, compared to naïve rats. Dietary administration of macitentan (5 mg/kg) significantly (p<0.01) enhanced the survival of RGCs (5% RGC loss), significantly (p<0.01) protected against optic nerve axonal injury and a trend towards preservation of PERG amplitude (not significant).

Conclusions : Blocking both ETA and ETB receptors by oral administration of the endothelin receptor antagonist, macitentan, may protect from hypoxic injury as well as promote RGC survival during ocular hypertension. Endothelin receptor antagonists could potentially act through both vascular and cellular mechanisms to promote neuroprotection in glaucoma.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×