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.