Complement peptide C3a receptor 1 promotes optic nerve degeneration in DBA/2J mice.

ABSTRACT:

Background

The risk of glaucoma increases significantly with age and exposure to elevated intraocular pressure, two factors linked with neuroinflammation. The complement cascade is a complex immune process with many bioactive end-products, including mediators of inflammation. Complement cascade activation has been shown in glaucoma patients and models of glaucoma. However, the function of complement-mediated inflammation in glaucoma is largely untested. Here, the complement peptide C3a receptor 1 was genetically disrupted in DBA/2J mice, an ocular hypertensive model of glaucoma, to test its contribution to neurodegeneration.

Methods

A null allele of C3ar1 was backcrossed into DBA/2J mice. Development of iris disease, ocular hypertension, optic nerve degeneration, retinal gan

SUBMITTER: Harder JM 

PROVIDER: S-EPMC7656757 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature