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A competitive PDLIM1-USP14 axis destabilizes ACTN4 to disturb the invasive homeostasis of trophoblast in preeclampsia.
Cell Reports · · Journal Article · Open access
Zhang, Zhang + more
Abstract ↗AI summary
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PDLIM1 is markedly upregulated in preeclampsia placenta and destabilizes ACTN4 by competitively displacing USP14, shifting ACTN4 toward RNF38-linked K48 ubiquitination and turnover.
- Why it matters: EVT invasion is insufficient in preeclampsia, but the cytoskeletal and proteostasis mechanisms that restrain trophoblast motility are not well defined.
- What they did: TMT-based placental proteomics identified PDLIM1 upregulation; PDLIM1 depletion remodeled actin and increased migration/invasion, while trophoblast-restricted Pdlim1 overexpression impaired invasion and placental development in mice.
- The result: Placenta-targeted chondroitin sulfate A-binding nanoparticles delivering Pdlim1 shRNA alleviated preeclampsia-like maternal and fetal phenotypes in mice, supporting PDLIM1 as a therapeutic target.
The findingWhy it mattersWhat they didThe result
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