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S14G-humanin (HNG) protects retinal endothelial cells from UV-B-induced NLRP3 inflammation activation through inhibiting Egr-1.
- Source :
- Inflammation Research; Dec2021, Vol. 70 Issue 10-12, p1141-1150, 10p
- Publication Year :
- 2021
-
Abstract
- UV-B stimulation can induce retinopathy, whose pathogenesis is currently unclear. UV-B mediated inflammation in retinal endothelial cells is reported to be involved in the pathogenesis of retinopathy. S14G-humanin (HNG) is a neuroprotective peptide that has recently been reported to exert significant anti-inflammatory effects and protective properties against cell death. The present study aims to investigate the protective effects of HNG against UV-B-challenged retinal endothelial cells and explore the underlying mechanism. UV-B radiation was used to induce an injury model in human retinal endothelial cells (HRECs). First, exposure to UV-B induced the expression of TXNIP. Additionally, we found that treatment with HNG inhibited the activation of the TXNIP/NLRP3 signaling pathway and mitigated the excessive release of IL-1β and IL-18 in UV-B-challenged HRECs. UV-B increased the expression of the transcriptional factor endothelial growth response-1 (Egr-1). Interestingly, overexpression of Egr-1 increased the luciferase activity of the TXNIP promoter as well as the mRNA and protein expression of TXNIP. In contrast, the knockdown of Egr-1 reduced the expression of TXNIP under both the normal and UV-B exposure conditions. Importantly, treatment with HNG attenuated UV-B-induced expression of Egr-1. However, overexpression of Egr-1 abolished the inhibitory effects of HNG-induced activation of NLRP3 as well as the production of IL-1β and IL-18. Taken together, our findings reveal that HNG protected retinal endothelial cells from UV-B-induced NLRP3 inflammation activation through inhibiting TXNIP mediated by Egr-1. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10233830
- Volume :
- 70
- Issue :
- 10-12
- Database :
- Complementary Index
- Journal :
- Inflammation Research
- Publication Type :
- Academic Journal
- Accession number :
- 153437855
- Full Text :
- https://doi.org/10.1007/s00011-021-01489-4