Key result
Treatment with HuMSC-EVs significantly improved cell viability and reduced ER stress-induced apoptosis in H9c2 cardiac cells exposed to hypoxia/reoxygenation injury via activation of the PI3K/Akt pathway.
Why the study?
Endoplasmic reticulum stress is implicated in myocardial ischemia/reperfusion injury, and whether human umbilical cord mesenchymal stromal cell-derived extracellular vesicles can protect cardiac cells against hypoxia/reoxygenation-induced stress was investigated.
Do HuMSC-EVs protect cardiac cells against hypoxia/reoxygenation injury by inhibiting ER stress?
Do HuMSC-EVs protect cardiac cells against hypoxia/reoxygenation injury by inhibiting ER stress?
p-value: p=<0.01
HuMSC-EVs protect H9c2 cardiac cells against hypoxia/reoxygenation injury by inhibiting ER stress-induced apoptosis via activation of the PI3K/Akt pathway in vitro.
Caution against clinical use of HuMSC-EVs; leaves open their cardioprotective potential in ischemia-reperfusion injury.
Endoplasmic reticulum (ER) stress is implicated in the pathogenesis of many diseases, including myocardial ischemia/reperfusion injury. We hypothesized that human umbilical cord mesenchymal stromal cells derived extracellular vesicles (HuMSC-EVs) could protect cardiac cells against hyperactive ER stress induced by hypoxia/reoxygenation (H/R) injury. The H/R model was generated using the H9c2 cultured cardiac cell line. HuMSC-EVs were extracted using a commercially available exosome isolation reagent. Levels of apoptosis-related signaling molecules and the degree of ER stress were assessed by western blot. The role of the PI3K/Akt pathway was investigated using signaling inhibitors. Lactate dehydrogenase leakage and 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) analysis were used for evaluating the therapeutic effects of HuMSC-EVs in vitro. The results showed that ER stress and the rate of apoptosis were increased in the context of H/R injury. Treatment with HuMSC-EVs inhibited ER stress and increased survival in H9c2 cells exposed to H/R. Mechanistically, the PI3K/Akt pathway was activated by treatment with HuMSC-EVs after H/R. Inhibition of the PI3K/Akt pathway by a specific inhibitor, LY294002, partially reduced the protective effect of HuMSC-EVs. Our findings suggest that HuMSC-EVs could alleviate ER stress–induced apoptosis during H/R via activation of the PI3K/Akt pathway.
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Zhang et al. (2020) studied Hypoxia/reoxygenation injury. Human umbilical cord mesenchymal stromal cells derived extracellular vesicles (HuMSC-EVs) vs. Hypoxia/reoxygenation without HuMSC-EVs was evaluated on Cell viability and apoptosis (p=<0.01). Treatment with HuMSC-EVs significantly improved cell viability and reduced ER stress-induced apoptosis in H9c2 cardiac cells exposed to hypoxia/reoxygenation injury via activation of the PI3K/Akt pathway.
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