| Autor: |
Man Shang, Yan-Xia Liu, Qian Zhu, Jun-Qiu Song, Ye-Yi Li, Yi-Lu Wang, Miao Liu, Yanna Wu, Junyu Zhao |
| Rok vydání: |
2020 |
| Předmět: |
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| DOI: |
10.21203/rs.2.24805/v1 |
| Popis: |
Background Microvesicles (MVs) are submicron membrane vesicles as mediators of intercellular communication. The aim of our study was to investigate protective mechanism of circulating MVs derived from ischemic preconditioning (IPC-MVs) on myocardial I/R injury. Results Administration of IPC-MVs reduced infarct size and activity of lactate dehydrogenase (LDH) in myocardial I/R injury in vivo. Meanwhile, IPC-MVs could increase cell viability and reduce LDH activity in hypoxia/reoxygenation (H/R) injured H9c2 cells in vitro. Microarray analysis demonstrated that miR-133a-3p expression in IPC-MVs increased apparently compared with Sham-MVs. We found that miR-133a-3p increased cell viability, decreased LDH activity and apoptosis , as well as suppressed H/R-induced endoplasmic reticulum stress (ERS). MVs induced by hypoxic preconditioning enriched with FAM-miR-133a-3p allowed the transfer of miR-133a-3p to target cells. In addition, miR-133a-3p was significantly increased in H/R injured H9c2 cells by treatment with IPC-MVs. Epidermal growth factor receptor (EGFR) is a target gene of miR-133a-3p. AG1478 (EGFR inhibitor) significantly increased cell viability, decreased LDH activity and ERS-induced apoptosis in H9c2 cells under H/R injury. Conclusions The findings of this study showed that IPC-MVs exerted cardioprotective effects by transferring miR-133a-3p into H/R injured cardiomyocytes targeting EGFR, thus attenuating ERS-induced apoptosis. MiR-133a-3p transferred by IPC-MVs may provide a novel therapy for myocardial I/R injury. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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