| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Zhang, Qi Shang, Man Zhang, Mengxiao Wang, Yao Chen, Yan Wu, Yanna Liu, Minglin Song, Junqiu Liu, Yanxia |
| Abstract | Background Vascular endothelial dysfunction is the closely related determinant of ischemic heart disease (IHD). Endothelial dysfunction and ischemia/reperfusion injury (IRI) have been associated with an increase in microvesicles (MVs) in vivo. However, the potential contribution of endothelial microvesicles (EMVs) to myocardial damage is unclear. Here we aimed to investigate the role of EMVs derived from hypoxia/reoxygenation (H/R) -treated human umbilical vein endothelial cells (HUVECs) on cultured H9c2 cardiomyocytes. Results H/R injury model was established to induce HUVECs to release H/R-EMVs. The H/R-EMVs from HUVECs were isolated from the conditioned culture medium and characterized. H9c2 cardiomyocytes were then incubated with 10, 30, 60 μg/mL H/R-EMVs for 6 h. We found that H9c2 cells treated by H/R-EMVs exhibited reduced cell viability, increased cell apoptosis and reactive oxygen species (ROS) production. Moreover mechanism studies demonstrated that H/R-EMVs could induce the phosphorylation of p38 and JNK1/2 in H9c2 cells in a dose-dependent manner. In addition, H/R-EMVs contained significantly higher level of ROS than EMVs generated from untreated HUVECs, which might be a direct source to trigger a cascade of myocardial damage. Conclusion We showed that EMVs released during H/R injury are pro-apoptotic, pro-oxidative and directly pathogenic to cardiomyocytes in vitro. EMVs carry ROS and they may impair myocardium by promoting apoptosis and oxidative stress. These findings provide new insights into the pathogenesis of IRI. |
| Related Links | https://bmcmolcellbiol.biomedcentral.com/counter/pdf/10.1186/s12860-016-0100-1.pdf |
| Ending Page | 10 |
| Page Count | 10 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 26618850 |
| DOI | 10.1186/s12860-016-0100-1 |
| Journal | BMC Molecular and Cell Biology |
| Issue Number | 1 |
| Volume Number | 17 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2016-06-23 |
| Access Restriction | Open |
| Subject Keyword | Cell Biology Biological Microscopy Life Sciences Endothelial microvesicles Oxidative stress Apoptosis H9c2 cardiomyocytes Hypoxia/reoxygenation |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Molecular Biology |
| Journal Impact Factor | 2.4/2023 |
| 5-Year Journal Impact Factor | 2.5/2023 |
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