ArticleExperimental and therapeutic medicine2019
Annexin A2 upregulation protects human retinal endothelial cells from oxygen-glucose deprivation injury by activating autophagy.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Multi-Omics Profiling Identifies Microglial Annexin A2 as a Key Mediator of NF-κB Pro-inflammatory Signaling in Ischemic Reperfusion Injury.Molecular & cellular proteomics : MCP · 2024Article
- Synthetic antibody-derived immunopeptide provides neuroprotection in glaucoma through molecular interaction with retinal protein histone H3.1.Frontiers in medicine · 2022Article
- Annexin A2 in Inflammation and Host Defense.Cells · 2020Review
- Stabilization of HIF-1α in Human Retinal Endothelial Cells Modulates Expression of miRNAs and Proangiogenic Growth Factors.Frontiers in pharmacology · 2020Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
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Abstract
Retinal neovascularization is a common pathological change in multiple diseases of the eyes and the upregulation of annexin A2 (A2) under a hypoxic and ischemic microenvironment has been demonstrated to be a key factor in the pathological process. However, the underlying mechanism by which A2 regulates retinal neovascularization remains unclear. In the present study, oxygen-glucose deprivation (OGD) was used to mimic the hypoxic and ischemic microenvironment, to observe the role of A2 in retinal neovascularization regulation by focusing on autophagy. The results showed that OGD treatment significantly increased the mRNA and protein levels of A2 in human retinal endothelial cells (HRECs), which was dependent on activation of hypoxia inducible factor (HIF)-1α signaling. The OGD-induced activation of autophagy was attenuated when A2 was silenced, but increased when A2 was overexpressed, suggesting that A2 upregulation contributed to OGD-induced cell autophagy activation. Furthermore, knockdown of A2 decreased cell viability and promoted cell apoptosis under OGD conditions. Overexpression of A2 increased cell viability and reduced cell apoptosis under OGD conditions, and inhibiting autophagy using an inhibitor, reversed these changes, suggesting that upregulation of A2 by OGD serves a cytoprotective role by inducing cell autophagy in HRECs. Taken together, the results of the present study suggested that promoting retinal endothelial cell survival by autophagy activation via the HIF-1α signaling pathway in a hypoxic and ischemic microenvironment may underlie the mechanism by which A2 regulates retinal neovascularization. The present study is the first study to demonstrate the novel role of A2 during retinal neovascularization under pathological conditions, to the best of our knowledge. Therefore, A2 may serve as a potential therapeutic target for treating neovascularization-associated conditions of the eye.
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