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EPC-EXs improve astrocyte survival and oxidative stress through different uptaking pathways in diabetic hypoxia condition
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EPC-EXs improve astrocyte survival and oxidative stress through different uptaking pathways in diabetic hypoxia condition
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Journal Article
EPC-EXs improve astrocyte survival and oxidative stress through different uptaking pathways in diabetic hypoxia condition
2022
Overview
Background
Hyperglycemia contributes to cardiovascular complications in patients with type 2 diabetes. We confirmed that high glucose (HG) induces endothelial dysfunction and cerebral ischemic injury is enlarged in diabetic mice. Stem cell-released exosomes have been shown to protect the brain from ischemic stroke. We have previously shown that endothelial progenitor cells (EPCs)-released exosomes (EPC-EXs) can protect endothelial cells from hypoxia/reoxygenation (H/R) and HG-induced injury. Here, we aim to investigate the effects of EPC-EXs on astrocytes under H/R and HG-induced injury and whether miR-126 enriched EPC-EXs (miR126-EPC-EXs) have enhanced efficacy.
Methods
EPC-EX uptake and co-localization were measured by fluorescent microscopy using PKH26 and DAPI staining. miR-126 enrichment was achieved by transfecting with miR-126 mimics and quantified with real-time PCR. After co-incubation, cell death or injury was measured by using LDH (Lactate Dehydrogenase) assay. Oxidative stress/ROS (reactive oxygen species) generation was measured by DHE (Dihydroethidium) staining and lipid peroxidation assay.
Results
The EPC-EXs were effectively taken up by the astrocytes in a concentration as well as time-dependent manners and were co-localized within the nucleus as well as the cytoplasm. Pathway uptake inhibitors revealed that the EPC-EXs are effectively taken up by the clathrin-mediated, caveolin-dependent, and micropinocytosis via PI3K/Akt pathway. H/R and HG-induced a cell injury which could be protected by EPC-EXs evidenced by decreased cell cytotoxicity, oxidative stress, and lipid peroxidation. Moreover, miR-126 overexpression could increase the level of miR-126 in astrocytes and enhance the protective effects of EPC-EXs.
Conclusions
These results collectively indicate that the EPC-EXs could protect astrocytes against the HG plus H/R-induced damage.
Publisher
BioMed Central,BioMed Central Ltd,BMC
Subject
/ Biomedical and Life Sciences
/ Biomedical Engineering and Bioengineering
/ Dextrose
/ Diabetes Mellitus, Experimental - metabolism
/ Diabetes Mellitus, Type 2 - metabolism
/ Endothelial progenitor cells
/ Endothelial Progenitor Cells - metabolism
/ Exosomes
/ Glucose
/ Humans
/ Hypoxia
/ Ischemia
/ Mice
/ Phosphatidylinositol 3-Kinases - metabolism
