Transplantation of adipose-derived stem cells may reduce renal ischemia/reperfusion induced tubular oxidative stress, apoptosis, autophagy and renal dysfunction. We suggest that pharmacological preconditioning adipose-derived stem cells-microvesicles may confer further protection against renal ischemia/reperfusion injury through microRNA mechanisms. Preconditioning adipose-derived stem cells with dexmedetomidine triggered higher migration capability than empagliflozin and N-acetylcysteine. Treatment of sonicating dexmedetomidine treated adipose-derived stem cells-microvesicles significantly preserved microcirculation and renal blood flow and decreased tubular injury score, pNF-κB-mediated inflammation, Beclin-1 mediated autophagy and caspase 3/poly (ADP-ribose) polymerase mediated apoptosis, blood urea nitrogen and creatinine levels vs. ischemia/reperfusion kidney and adipose-derived stem cells-microvesciles treated kidney. Post-ischemia/reperfusion kidneys had higher levels of miR-122-5p expression and lower levels of miR-543-3p expression vs. control kidney. Dexmedetomidine treated adipose-derived stem cells-microvesicles treatment significantly preserved ischemia/reperfusion altered miR-122-5p and miR-543-3p expression in the ischemia/reperfusion kidney. In the HOCl injuried NRK52E cells, exogenous miR-122-5p mimics exacerbated and miR-543-3p mimics ameliorated Bax/Bcl-2 mediated apoptosis and Beclin-1 mediated autophagy. In conclusion, upregulation of miR-122-5p expression and downregulation of miR-543-3p in the post-ischemia/reperfusion kidney may contribute a role in tubular cell apoptosis and autophagy and renal dysfunction. Dexmedetomidine treated adipose-derived stem cells-microvesicles reduced renal ischemia/reperfusion injury through restoring miR-122-5p and miR-543-3p mediated apoptosis and autophagy.
|Effective start/end date||2017/08/01 → 2020/07/31|
- adipose-derived mesenchymal stem cells
- programmed cell death
- reactive oxygen species
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