Botulinum neurotoxin serotype A inhibited ocular angiogenesis through modulating glial activation via SOCS3.

ABSTRACT:

Background

Pathological angiogenesis causes significant vision loss in neovascular age-related macular degeneration and other retinopathies with neovascularization (NV). Neuronal/glial-vascular interactions influence the release of angiogenic and neurotrophic factors. We hypothesized that botulinum neurotoxin serotype A (BoNT/A) modulates pathological endothelial cell proliferation through glial cell activation and growth factor release.

Methods

A laser-induced choroidal NV (CNV) was employed to investigate the anti-angiogenic effects of BoNT/A. Fundus fluorescence angiography, immunohistochemistry, and real-time PCR were used to assess BoNT/A efficacy in inhibiting CNV and the molecular mechanisms underlying this inhibition. Neuronal and glial suppressor of cytokine signali

SUBMITTER: Gregg AT 

PROVIDER: S-EPMC11564384 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature