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Purification and Transplantation of Myogenic Progenitor Cell Derived Exosomes to Improve Cardiac Function in Duchenne Muscular Dystrophic Mice
Published on: April 10, 2019
Exosomal transfer of miR-30a between cardiomyocytes regulates autophagy after hypoxia
Yan Yang1, Yingying Li1, Xiao Chen1
1Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430022, China.
Unlabelled:
Recent studies have indicated a protective role of physiological autophagy in ischemic heart disease. However, the underlying mechanisms of autophagy regulation after ischemia are poorly understood. Exosomes are nano-sized vesicles released from cells that play critical roles in mediating cell-to-cell communication through the transfer of microRNAs. In this study, we observed that miR-30a was highly enriched in exosomes from the serum of acute myocardial infarction (AMI) patients in vivo and culture medium of cardiomyocytes after hypoxic stimulation in vitro. We also found that hypoxia inducible factor (HIF)-1α regulates miR-30a, which efficiently transferred via exosomes between cardiomyocytes after hypoxia. Inhibition of miR-30a or release of exosomes increased the expression of the core autophagy regulators beclin-1, Atg12, and LC3II/LC3I, which contributed to maintaining the autophagic response in cardiomyocytes after hypoxia. Taken together, the present study showed that exosomes from hypoxic cardiomyocytes regulate autophagy by transferring miR-30a in a paracrine manner, which revealed a new pathway of autophagy regulation that might comprise a promising strategy to treat ischemic heart disease.
Key Messages:
miR-30a is highly enriched in exosomes from the serum of AMI patients. Hypoxia induces miR-30a upregulation and enrichment into exosomes. MiR-30a is efficiently transferred via exosomes between hypoxic cardiomyocytes. Inhibition of exosome release contributes to maintaining of autophagy after hypoxia. Inhibition of miR-30a augments autophagy after hypoxia.
Insights
Exosomes carrying miR-30a from hypoxic heart cells regulate autophagy. Inhibiting miR-30a or exosome release enhances autophagy, offering a potential treatment for ischemic heart disease.
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Biochemistry
Background:
- Autophagy plays a protective role in ischemic heart disease, but its regulation post-ischemia is unclear.
- Exosomes mediate cell-to-cell communication via microRNA transfer.
- Understanding exosome-mediated regulation of autophagy is crucial for treating heart disease.
Purpose of the Study:
- To investigate the role of exosomal miR-30a in regulating autophagy in cardiomyocytes after hypoxia.
- To elucidate the mechanism by which hypoxia-induced exosomes affect autophagy.
- To explore potential therapeutic strategies for ischemic heart disease.
Main Methods:
- Quantified miR-30a enrichment in exosomes from acute myocardial infarction (AMI) patients and hypoxic cardiomyocytes.
- Investigated the regulation of miR-30a by hypoxia-inducible factor (HIF)-1α.
- Assessed the transfer of miR-30a via exosomes between cardiomyocytes.
- Measured autophagy regulators (beclin-1, Atg12, LC3II/LC3I) after inhibiting miR-30a or exosome release.
Main Results:
- miR-30a was highly enriched in exosomes from AMI patients and hypoxic cardiomyocytes.
- Hypoxia induced miR-30a upregulation and its packaging into exosomes, mediated by HIF-1α.
- Exosomes efficiently transferred miR-30a between cardiomyocytes, suppressing autophagy.
- Inhibition of miR-30a or exosome release enhanced autophagy by increasing beclin-1, Atg12, and LC3II/LC3I expression.
Conclusions:
- Hypoxic cardiomyocytes release exosomes containing miR-30a, which suppresses autophagy in a paracrine manner.
- This exosome-miR-30a pathway represents a novel mechanism for autophagy regulation in ischemic conditions.
- Targeting exosomal miR-30a may offer a promising therapeutic strategy for ischemic heart disease.
