DEL-1: a promising treatment for AMD-associated ER stress in retinal pigment epithelial cellsopen access
- Authors
- Kwon, ChangHyuk; Cho, Wonjun; Choi, Sung Woo; Oh, Heeseung; Abd El-Aty, A.M.; Gecili, Ibrahim; Jeong, Ji Hoon; Jung, Tae Woo
- Issue Date
- Jan-2024
- Publisher
- BioMed Central Ltd
- Keywords
- AMD; Apoptosis; Autophagy; DEL-1; ER stress; Retinal pigment epithelial cells
- Citation
- Journal of Translational Medicine, v.22, no.1
- Journal Title
- Journal of Translational Medicine
- Volume
- 22
- Number
- 1
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/72683
- DOI
- 10.1186/s12967-024-04858-9
- ISSN
- 1479-5876
1479-5876
- Abstract
- Background: Age-related macular degeneration (AMD) is an irreversible eye disease that can cause blurred vision. Regular exercise has been suggested as a therapeutic strategy for treating AMD, but how exercise improves AMD is not yet understood. This study investigated the protective effects of developmental endothelial locus-1 (DEL-1), a myokine upregulated during exercise, on endoplasmic reticulum (ER) stress-induced injury in retinal pigment epithelial cells. Methods: We evaluated the levels of AMPK phosphorylation, autophagy markers, and ER stress markers in DEL-1-treated human retinal pigment epithelial cells (hRPE) using Western blotting. We also performed cell viability, caspase 3 activity assays, and autophagosome staining. Results: Our findings showed that treatment with recombinant DEL-1 dose-dependently reduced the impairment of cell viability and caspase 3 activity in tunicamycin-treated hRPE cells. DEL-1 treatment also alleviated tunicamycin-induced ER stress markers and VEGF expression. Moreover, AMPK phosphorylation and autophagy markers were increased in hRPE cells in the presence of DEL-1. However, the effects of DEL-1 on ER stress, VEGF expression, and apoptosis in tunicamycin-treated hRPE cells were reduced by AMPK siRNA or 3-methyladenine (3-MA), an autophagy inhibitor. Conclusions: Our study suggests that DEL-1, a myokine, may have potential as a treatment strategy for AMD by attenuating ER stress-induced injury in retinal pigment epithelial cells. © 2024, The Author(s).
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