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Related Experiment Videos

Latrunculin-A increases outflow facility in the monkey.

J A Peterson1, B Tian, A D Bershadsky

  • 1Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, USA.

Investigative Ophthalmology & Visual Science
|April 2, 1999
PubMed
Summary
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Latrunculin-A disrupts endothelial cell actin and increases outflow facility in monkeys, suggesting potential as an antiglaucoma treatment by targeting the actin cytoskeleton.

Area of Science:

  • Cell Biology
  • Ocular Physiology
  • Pharmacology

Background:

  • The actin cytoskeleton plays a crucial role in maintaining cell shape and adhesion.
  • Disruptions in the actin cytoskeleton are implicated in various cellular processes and disease states.
  • Understanding how actin-disrupting agents affect endothelial cells and ocular structures is important for therapeutic development.

Purpose of the Study:

  • To investigate the effects of Latrunculin-A (LAT-A) on the actin cytoskeleton, cell shape, and junctions of cultured bovine aortic endothelial cells (BAECs).
  • To evaluate the impact of LAT-A on outflow facility in living monkeys.
  • To explore the potential of LAT-A as an antiglaucoma strategy.

Main Methods:

  • Dose- and time-response studies of LAT-A in BAECs using immunofluorescence and phase contrast microscopy.

Related Experiment Videos

  • Anterior chamber perfusion in monkeys to measure outflow facility changes.
  • Assessment of drug-induced cytoskeletal disorganization and cell adhesion alterations.

    • Main Results:

    • LAT-A caused dose- and time-dependent disruption of actin bundles, cell separation, and loss in BAECs, with cell-cell adhesions being more sensitive than focal contacts.
    • Intracameral and topical LAT-A administration in monkeys resulted in significant, reversible increases in outflow facility.
    • A single topical LAT-A dose led to an accelerated facility increase beyond normal resistance washout for at least 24 hours.

    Conclusions:

    • Pharmacological disruption of the actin cytoskeleton in the trabecular meshwork using agents like LAT-A shows promise as an antiglaucoma strategy.
    • LAT-A effectively alters endothelial cell structure and increases ocular outflow facility.
    • Targeting the actin cytoskeleton represents a potential therapeutic avenue for managing glaucoma.