What is it about?
Endothelial dysfunction is an indicator of kidney damage after LPS injection (AKI). Endothelial cells (ECs), via the endothelial-to‐mesenchymal transition (EndMT) phase, contribute to the development of the fibrosis. Human adult renal stem/progenitor cells (ARPCs) stabilized the EC proliferation rate and inverted the LPS-induced EndMT. The ARPC-specific antifibrotic effect is due to the secretion of CXCL6, SAA4, and BPIFA2 antiseptic peptides after the stimulation of LPS. Finally, in the pig model of the LPS-induced AKI, the activated ARPC secreted CXCL6, SAA4, and BPIFA2 as a defense response.
Photo by National Cancer Institute on Unsplash
Why is it important?
We demonstrated for the first time that ARPCs can preserve endothelial phenotype by preventing the development of the LPS-induced EndMT process. We identified the secretion of CXCL6, SAA4, and BPIFA2 antiseptic peptides as the principal mechanism that can counteract the effect of LPS in our model. These data open new perspectives on the treatment of both sepsis- and endotoxemia-induced AKI, suggesting an underestimated role of ARPCs in preventing endothelial dysfunction and novel strategies to protect the endothelial compartment and promote kidney repair.
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This page is a summary of: Renal progenitor cells revert LPS‐induced endothelial‐to‐mesenchymal transition by secreting CXCL6, SAA4, and BPIFA2 antiseptic peptides, The FASEB Journal, July 2019, Wiley, DOI: 10.1096/fj.201900351r.
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