GSE212273
Analyze the mechanism of polyploidization of proximal tubular cells (PTC) in the unilateral ischemia reperfusion injury model of acute kidney injury (AKI) in mice
We found that PTC undergo polyploidization immediately after AKI induced by ischemia. To identify the mechanism controlling polyploidization of PTC, we generated single-cell RNA sequencing (scRNAseq) datasets from healthy mouse kidneys, 2 and 30 days after ischemia reperfusion injury.  We found that polyploid PTC become hypertrophic and undergo polyploidization in a YAP1-related manner. In particular, YAP1 controls polyploidization of PTC via E2f7, E2f8 and Akt1. We confirmed these findings by knocking-down those genes in vitro. Overall design: Identify and characterize the mechanism controlling the polyploidization process of PTC after Acute Kidney Injury