LE MICROVESCICOLE DERIVATE DA CELLULE STAMINALI MESENCHIMALI GLOMERULARI ACCELLERANO LA RIPRESA FUNZIONALE DOPO DANNO DA ISCHEMIA RIPERFUSIONE

[Machine translation] introduction. Bone marrow—derived mesenchymal stem cells (MSCs) accelerate functional recovery after acute kidney injury (AKI) with a paracrine mechanism. The microvesicles (MVs) released by MSCs are partly responsible for the paracrine effect through the transfer of mRNA. We isolated MSCs from human glomeruli (GL-MSCs) co-expressing stem and kidney markers. GL-MSCs can differentiate into mesangial and endothelial cells, suggesting a role in glomerular cell turnover. The purpose of the study was to evaluate whether MVs derived from GL-MSCs accelerate functional recovery in , a mouse model of ischemia-reperfusion (I/R) damage. , Materials and Methods. In 3 groups (8/group) of SCID mice, 15 mcg of MVs and MVs inactivated with RNase (MVRs) or vehicle (CTL) were administered respectively immediately after surgery. I/R damage (35 minutes of clamping of the left renal vascular peduncle) has been associated with right nephrectomy. afterward , Mice were sacrificed for 48 hours and plasma creatinine (SCRs) and BUN were dosed. Renal damage (presence of intraluminal cylinders and tubular necrosis), proliferation such as BrdU incorporation and PCNA expression, and apoptosis using TUNEL were evaluated by morphometric analysis., Results. MVs improve functional recovery after I/R damage (SCRs MVs vs CTL: 0.7±0.21 vs 1.3±0.3, p<0.05). Renal damage is reduced in the group with MVs compared to the CTL group (cylinders/HPF: 1.3±0.7 vs 4.7±1.1, p<0.05; necrotic tubules/HPF: 7.6±1.5 vs 11.7±1.5, p<0.05). Cell proliferation , It increased in the MVs group compared to the CTL group (positive PCNA nuclei/, HPF: 21.9±3.1 vs 12±1.4, p<0.05; BrdU positive/HPF 17.7±3.8 vs 8±2.4, p<0.05). These effects are reduced by RNase treatment of MVs., Conclusions. The results of the study demonstrate that GL-MSC-derived MVs improve the recovery of kidney function after I/R damage by promoting the proliferation of tubular cells