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- Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton . . .
For this purpose, we treated a human RPE cell line (ARPE-19) with sodium iodate (SI), an oxidative stress agent, together with dimethyloxalylglycine (DMOG) which leads to stabilization of hypoxia-inducible factors (HIFs), key regulators of cellular adaptation to hypoxic conditions
- Placental growth factor promotes epithelial-mesenchymal transition-like . . .
Thus, in the present study, we investigated the role of PGF in the EMT of ARPE-19 cells under hypoxia Moreover, we demonstrated that the NF-κB signaling pathway could regulate this process
- Real-Time Monitoring the Effect of Cytopathic Hypoxia on . . . - PubMed
Our data demonstrate that the ARPE-19 cells have distinct dielectric properties in response to cytopathic hypoxia in which disruption of barrier integrity between ARPE-19 cells precedes any changes in cells' viability, cell-substrate contacts, and cell membrane permeability
- Hypoxia induces an inflammatory response in ARPE-19 cells
An acute exposure to hypoxia induced an inflammatory response in ARPE-19 cell culture as characterized with an increased IL-6 and IL-8 secretion from cell culture
- Glaucine inhibits hypoxia-induced angiogenesis and attenuates LPS . . .
Our results revealed that glaucine exhibits anti-angiogenic and anti-inflammatory effects on hypoxia- and LPS-induced ARPE-19 cells, suggesting it might have therapeutic potential in treating AMD
- Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton . . .
For this purpose, we treated a human RPE cell line (ARPE-19) with sodium iodate (SI), an oxidative stress agent, together with dimethyloxalylglycine (DMOG) which leads to stabilization of
- Nrf2 and Hif1a have opposite responses to oxidative stress in ARPE-19 . . .
Abstract Purpose : Smoking causes oxidative stress and damage to the retina, reduces blood flow in eye tissue, and promotes ischemia, hypoxia, and micro-infarctions It also induces cell death to retinal pigment epithelial (RPE) cells
- Phosphorylation of STAT3 and ERBB2 mediates hypoxia-induced VEGF . . .
Therefore, the RPE-derived human cell line ARPE-19 was exposed to hypoxia Hypoxia-induced phosphorylation of STAT3 and ERBB2 in ARPE-19 cells was decreased by AG490, an inhibitor of Janus kinase 2, as were hypoxia-induced VEGF release and tube formation in human umbilical vein endothelial cells
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