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PAC-Mediated AKI Protection Is Critically Mediated but Does Not Exclusively Depend on Cell-Derived Microvesicles
H Dihazi1, K Schwarze1, S Patschan2
1Klinik für Nephrologie und Rheumatologie, Universitätsmedizin Göttingen, Göttingen, Germany.
International Journal of Nephrology
|March 29, 2021
Summary
Proangiogenic cells (PACs) protect against acute kidney injury (AKI), primarily through their microvesicles (MV). However, combining MV with certain preconditioning agents worsened kidney function, suggesting complex protective mechanisms beyond just MV.
Area of Science:
- Nephrology
- Regenerative Medicine
- Cell Biology
Background:
- Acute kidney injury (AKI) is a critical condition in hospitalized patients.
- Cell-based therapies, particularly using proangiogenic cells (PACs), show promise for AKI treatment.
- PACs exert protective effects partly through extracellular vesicles (microvesicles, MV) and their secretome.
Purpose of the Study:
- To investigate whether PAC-derived MV and/or secretome alone can prevent AKI.
- To determine the role of MV in PAC-mediated AKI protection.
Main Methods:
- AKI was induced in mice via renal ischemia-reperfusion injury (IRI).
- PACs were stimulated with melatonin, angiopoietin-1/-2, or BMP-5.
- PAC-derived MV and vesicle-depleted supernatant (secretome) were isolated and administered intravenously post-ischemia.
Main Results:
- Ischemia-reperfusion injury significantly impaired kidney function, indicated by elevated serum cystatin C.
- Only MV from native PACs improved AKI outcomes.
- Co-administration of MV with Ang-1, BMP-5, melatonin, or secretome+Ang-1 exacerbated kidney dysfunction.
Conclusions:
- PAC-mediated AKI protection is significantly dependent on cell-derived MV.
- The exacerbation of AKI when MV were combined with certain preconditioning agents suggests non-vesicle-dependent mechanisms are also involved in PAC-mediated protection.
- Further research is needed to elucidate the complex interplay of factors in PAC-based AKI therapy.
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