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Bone Marrow Mesenchymal Stem Cell-Derived Exosomes microRNA-31-5p Repress Pulmonary Fibrosis via IGFBP7
Lingrui Zhang1, Ke Qiu1, Chenchen Zhang2
1School of Nursing and Health Care, Leshan Vocational and Technical College, Leshan, China.
Abstract:
Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exos) with their molecular cargo have therapeutic potential for pulmonary fibrosis (PF). This research was performed to uncover how microRNA-31-5p (miR-31-5p), carried by BMSCs-Exos, affects PF via modulating IGFBP7. C57BL/6 mice were treated with bleomycin (BLM) to induce PF. Pulmonary function was tested, and fibrotic changes in the mouse lung tissues were examined. Levels of fibrosis-related inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, were tested. Mouse BMSCs were isolated and identified, and BMSCs-Exos were obtained by ultracentrifugation. Exosome morphology was observed by transmission electron microscopy, the surface markers were measured, and the expression levels of BMSCs-Exo marker proteins were assessed. The targeting relation between miR-31-5p and IGFBP7 was assessed, and the expression of both was tested. After modeling, mice exhibited decreased functional residual capacity, lung compliance, inspiratory capacity, vital capacity, total lung capacity, and forced vital capacity. After 14 days of BLM induction, thickening of the main tracheal wall, fibroblast accumulation, immune cell infiltration in lung interstitium, and increased collagen deposition were observed. Elevated levels of TNF-α, IL-1β, and IL-6 were also noted. BMSCs-Exos attenuated BLM-induced PF, and BMSCs-Exo-derived miR-31-5p ameliorated PF in mice. miR-31-5p was shown to target IGFBP7, diminishing both transcript and protein levels. IGFBP7 overexpression reversed the ameliorative impact of miR-31-5p on PF in mice. BMSCs-Exos ameliorate PF development by delivering miR-31-5p to repress IGFBP7.
Insights
Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exos) deliver microRNA-31-5p (miR-31-5p) to treat pulmonary fibrosis (PF). This microRNA targets IGFBP7, reducing fibrosis and inflammation in mice.
Area of Science:
- Regenerative Medicine
- Molecular Biology
- Pulmonary Medicine
Background:
- Pulmonary fibrosis (PF) is a debilitating lung disease with limited treatment options.
- Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exos) show therapeutic promise for PF due to their molecular cargo.
- The specific mechanisms by which BMSCs-Exos exert their effects in PF require further elucidation.
Purpose of the Study:
- To investigate the role of microRNA-31-5p (miR-31-5p), carried by BMSCs-Exos, in the pathogenesis and treatment of pulmonary fibrosis.
- To determine if miR-31-5p modulates Insulin-like Growth Factor Binding Protein 7 (IGFBP7) in the context of PF.
- To evaluate the therapeutic potential of BMSCs-Exos and miR-31-5p in a bleomycin-induced mouse model of PF.
Main Methods:
- Pulmonary fibrosis was induced in C57BL/6 mice using bleomycin (BLM).
- Pulmonary function tests and histological examination of lung tissues were performed.
- BMSCs were isolated, identified, and BMSCs-Exos were characterized using transmission electron microscopy and surface marker analysis.
- The expression levels of miR-31-5p and IGFBP7 were measured, and their targeting relationship was assessed.
- Mice were treated with BMSCs-Exos, and the effects of miR-31-5p and IGFBP7 overexpression were evaluated.
Main Results:
- BLM-induced PF in mice resulted in impaired pulmonary function, increased lung collagen deposition, and elevated levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
- BMSCs-Exos treatment attenuated BLM-induced PF, improving lung function and reducing fibrotic markers.
- BMSCs-Exo-derived miR-31-5p was found to directly target and downregulate both the transcript and protein levels of IGFBP7.
- Overexpression of IGFBP7 reversed the protective effects of miR-31-5p on PF.
Conclusions:
- BMSCs-Exos ameliorate pulmonary fibrosis development in mice.
- The therapeutic effect of BMSCs-Exos in PF is mediated, at least in part, by the delivery of miR-31-5p.
- miR-31-5p exerts its antifibrotic effects by repressing IGFBP7 expression, highlighting a novel therapeutic pathway for PF.
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