Extracellular vesicles derived from HBMSCs improved myocardial infarction through inhibiting zinc finger antisense 1 and activating Akt/Nrf2/HO-1 pathway
| Autor: | Huiling Xiao, Dan Wu, Tao Yang, Wei Fu, Lu Yang, Chenkai Hu, Hongbing Wan, Xiaomin Hu, Chenjie Zhang, Tao Wu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: |
Male
HBMSCs NF-E2-Related Factor 2 HO-1 Myocardial Infarction Bioengineering Transfection Applied Microbiology and Biotechnology Nrf2 Extracellular Vesicles Cell Movement Animals Humans Myocytes Cardiac EVs Cells Cultured Cell Proliferation Akt ZFAS1 Mesenchymal Stem Cells General Medicine Cell Hypoxia Rats Disease Models Animal Heme Oxygenase (Decyclizing) vWF RNA Long Noncoding Proto-Oncogene Proteins c-akt TP248.13-248.65 Biotechnology Research Article Research Paper Signal Transduction |
| Zdroj: | Bioengineered article-version (VoR) Version of Record Bioengineered, Vol 13, Iss 1, Pp 905-916 (2022) |
| ISSN: | 2165-5987 2165-5979 |
| Popis: | Myocardial infarction (MI) is believed to be one of the most common cardiovascular diseases, and it is seriously threatening the health of people in the world. The extracellular vesicles (EVs) isolated from mesenchymal stem cells and zinc finger antisense 1 (ZFAS1) have been believed to be involved in the regulation of MI, but the mechanism has not been fully clarified. Left anterior descending artery ligation was used to establish MI animal model, hypoxia treatment was applied to establish MI cell model. CCK8, transwell, and wound healing methods were applied to measure cell proliferation, invasion, and migration. Overexpression of ZFAS1 was established via transfecting pcDNA-ZFAS1. Overexpression of ZFAS1 significantly reversed the influence of EVs on cell migration, invasion, and apoptosis. Similar effect of EVs and ZFAS1 on morphological changes of MI rat heart tissues were also observed. The activation of Akt/Nrf2/HO-1 pathway by EVs was remarkably suppressed by pcDNA-ZFAS1. Inhibitor of Akt/Nrf2/HO-1 pathway remarkably reversed the impact of EVs on the cell viability. EVs might improve MI through inhibiting ZFAS1 and promoting Akt/Nrf2/HO-1 pathway. This study might provide a new thought for the prevention and treatment of MI damage through regulating ZFAS1 or Akt/Nrf2/HO-1 pathway. |
| Databáze: | OpenAIRE |
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