June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
The regulation of cGAS-STING signaling by PPARα-mediated autophagy in ischemic retinopathy
Author Affiliations & Notes
  • Xiang Ma
    Physiology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States
  • Yusuke Takahashi
    Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
  • Jiyang Cai
    Physiology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States
  • Jian-Xing Ma
    Physiology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States
    Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
  • Footnotes
    Commercial Relationships   Xiang Ma None; Yusuke Takahashi None; Jiyang Cai None; Jian-Xing Ma None
  • Footnotes
    Support  NH Grant EY019309, EY012231, EY028949, EY032930, and EY032931
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 4601 – F0393. doi:
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    • Get Citation

      Xiang Ma, Yusuke Takahashi, Jiyang Cai, Jian-Xing Ma; The regulation of cGAS-STING signaling by PPARα-mediated autophagy in ischemic retinopathy. Invest. Ophthalmol. Vis. Sci. 2022;63(7):4601 – F0393.

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

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Abstract

Purpose : Ischemia-induced retinopathy is one of the leading causes of irreversible blindness. Overactivated retinal myeloid cells are a crucial driving force of pathological angiogenesis and inflammation in ischemic retinopathy. The cyclic GMP-AMP (cGAMP) synthase (cGAS) and stimulator of interferon genes (STING) pathway is a key regulator of myeloid cell activation. This study investigated both the functions and regulatory mechanisms of cGAS-STING signaling in oxygen-induced retinopathy (OIR).

Methods : WT C57BL/6J mice and Sting-/- mice were used for OIR. Retinal neovascular and avascular areas were quantified in isolectin-stained retinal flat mounts. Retinal leukocyte adhesion was measured by perfusion labeling with concanavalin A lectin. Retinal myeloid cells were isolated from retinas using CD11b+ MACS microbeads. The cGAS, STING, peroxisome proliferator-activated receptor α (PPARα), and autophagy markers were measured using Western blot analysis. Surface and activation markers of retinal myeloid cells were measured by flow cytometry.

Results : The protein levels of cGAS-STING signaling were markedly upregulated in retinal CD11b+ cells of OIR mice. Sting knockout (KO) alleviated pathologies of OIR, including retinal neovascular areas, avascular areas, and leukostasis. Sting KO reduced the percentages of active M1 (IL1β+) and M2 (CD163) myeloid cells in OIR retinas. In addition, we found that PPARα was downregulated in retinal CD11b+ cells of the OIR model. Pparα-/- mice showed higher cGAS-STING levels in retinal CD11b+ cells compared to those in WT mice. PPARα agonists suppressed cGAS-STING signaling in the OIR retinas and mitigated the pathologies of OIR. In primary retinal microglial cells, the cGAS-STING levels were decreased in cells with starvation-induced autophagy and increased when autophagy was blocked by chloroquine. Pparα-/- retinal microglial cells showed defective autophagy and increased protein levels of cGAS-STING. Induction of autophagy decreased cGAS-STING levels in Pparα-/- retinal microglial cells.

Conclusions : Overactivation of cGAS-STING signaling in retinal myeloid cells plays a pathogenic role in ischemic retinopathy. PPARα inhibits the overactivated cGAS-STING signaling via the modulation of autophagy.

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

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