TP53BP2 silencing attenuates PE progression by reducing autophagy in rats
On the basis of these in vitro findings, we established a PE model by inducing RUPP in rats on the 14th day of gestation to investigate the role of TP53BP2 (Figure 2A-D ). Knockdown of TP53BP2 via the use of recombinant adeno-associated virus serotype 9 vectors carrying TP53BP2 shRNA (AAV-shTP53BP2) in PE rats resulted in decreased blood pressure (Figure 2E ) and proteinuria (Figure 2F ) and increased fetal weight (Figure 2G ). HE staining also revealed a reduction in both hydropic degeneration of decidual cells and deposition of fibrous proteins in this rat model (Figure 2H ). Furthermore, placentas from preeclamptic rats with downregulated TP53BP2 presented reduced LC3B-II expression and increased p62 expression (Fig 2I). Similar results were observed by immunofluorescence staining (Figure 2J ). Additionally, immunohistochemical staining revealed a significant reduction in LC3B expression and upregulation of p62 expression in placentas from preeclamptic rats subjected to TP53BP2 knockdown (Figure 2K ). Collectively, these results suggest that TP53BP2 knockdown attenuated autophagy in trophoblasts in the placenta of preeclamptic rats.