EPO-modified bone marrow MSCs alleviate asthma inflammation through enhanced mitochondrial activation and transfer by upregulating HO-1

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

BACKGROUND: Bone marrow mesenchymal stem cells (BM-MSCs) can rejuvenate injured cells through mitochondrial transfer. Our previous study has highlighted the ability of erythropoietin (EPO)-modified BM-MSCs (EPO-BM-MSCs) to relieve asthmatic inflammation. Here, we elucidated whether EPO-BM-MSCs improve asthmatic phenotype by mitochondrial transfer and investigated the underlying mechanism. METHODS: EPO-BM-MSCs and different modified EPO-BM-MSCs were generated. Ovalbumin (OVA)-induced asthma mouse models were established, and mtCC1-2 cells were treated with CoCl2 to mimic in vitro asthmatic phenotype. EPO-BM-MSC engraftment and mitochondrial transfer from EPO-BM-MSCs to epithelial cells were assessed by fluorescent microscopy and flow cytometry. Mitochondrial membrane potential, ROS production and tunnelling nanotube (TNT) formation were detected by flow cytometry or fluorescent microscopy. RESULTS: Intratracheal transplantation of EPO-BM-MSCs alleviated airway inflammation, asthmatic phenotype, and mitochondrial dysfunction in the lungs of OVA-induced asthma mice. Moreover, EPO-BM-MSCs had more efficient effects than BM-MSCs. EPO-BM-MSCs diminished CoCl2-triggered mitochondrial dysfunction in mtCC1-2 cells in vitro, which could be reversed by the inhibitors of TNT formation. When CoCl2-stimulated mtCC1-2 cells were co-cultured with EPO-BM-MSCs, TNT formation significantly increa

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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