Human renal stem/progenitor cells repair tubular epithelial cell injury through TLR2-driven inhibin-A and microvesicle-shuttled decorin

摘要: Acute kidney injury (AKI) is emerging as a worldwide public health problem. Recent studies have focused on the possibility of using human adult renal stem/progenitor cells (ARPCs) to improve repair AKI. Here we studied influence ARPCs healing cisplatin-injured proximal tubular epithelial cells. Tubular, but not glomerular, provided protective effect promoting proliferation surviving and inhibiting cisplatin-induced apoptosis. The recovery was specific ARPCs, occurred only after damage sensing, completely cancelled by TLR2 blockade ARPCs. Moreover, tubular, were resistant apoptotic cisplatin. Tubular operate mainly through engagement TLR2, secretion inhibin-A protein, microvesicle-shuttled decorin, inhibin-A, cyclin D1 mRNAs. These factors worked synergistically essential process. involvement ARPC-secreted decorin mRNA in pathophysiology AKI also confirmed transplant patients affected delayed graft function. Hence, identification this TLR2-driven mechanism may shed light new therapeutic strategies promote capacity acute damage. Use these components, derived from avoids injecting stem