Persistent cerebrovascular injury after preeclampsia in the STOX1A mouse model: implications for prokineticin signaling

In the STOX1A mouse model of preeclampsia, prokineticin signaling is linked to persistent cerebrovascular injury at 7–8 months postpartum, with PC1 preventing focal lesions.

• Why it matters: Preeclampsia-associated neurological complications can outlast pregnancy, but the maternal brain prokineticin pathway and whether blocking its receptors limits lasting injury are unclear.
• What they did: Female FVB/N mice mated with STOX1A-overexpressing males received PC1 or vehicle during gestation; circulating and regional PROK1/PROK2 and PROKR1/PROKR2 were measured, and brains were assessed by high-resolution MRI and GFAP staining at 7–8 months.
• The result: PE increased circulating PROK1 and PROK2 and produced hippocampal and parieto-temporal T2* hypointensities and post-contrast T1 abnormalities; PC1 prevented hypertension, reduced circulating PROKs, and prevented focal cerebral lesions and astrocyte reactivity, while regional diffusion abnormalities persisted.

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