Abstract
Purpose :
Explore the retinal microglial function in disease contexts.
Methods :
Microglia polarity was investigated from 6 h to 3 days after light damage(LD) and were analyzed in published mouse bulk RNA and single-cell sequencing (sc-RNA) databases. High-content image analysis and molecular analysis were conducted to determine microglia reactivity. Retinal morphology, function and inflammatory responses were assessed in response to IVTA administration.
Results :
LD induced a proinflammatory M1 microglial signature, and M1 marker proteins were elevated in a time-dependent manner in theretina after LD. IVTA treatment inhibited LD-induced retinal inflammation，retinal blood vessel leakage and protected retinal responsiveness and visual behavior after LD. Mechanistically, TA inhibited the proinflammatory phenotype but promoted the anti-inflammatory microglial phenotype by activating STAT6/Arg1 signaling.
Conclusions :
We revealed a new mechanism by which TA protects the retina against LD by shifting
microglia to an anti-inflammatory phenotype by activating the STAT6/Arg1 pathway.
This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.