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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Published on: January 26, 2024

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PP038. Renal ETK/BMX activation decreased in preeclampsia

Helena Strevens, Dag Wide-Swensson, Ola Hansson

    Pregnancy Hypertension
    |June 25, 2015
    PubMed
    Abstract

    Insights

    Preeclampsia is linked to reduced levels of phosphorylated ETK/BMX, a key mediator of vascular endothelial growth factor (VEGF) signaling in the kidneys. This suggests a potential role for ETK/BMX in preeclampsia pathophysiology.

    Area of Science:

    • Renal physiology and pathophysiology
    • Molecular biology of pregnancy disorders

    Background:

    • Vascular endothelial growth factors (VEGFs) are crucial for blood vessel formation (angiogenesis) and are implicated in preeclampsia.
    • Antagonizing VEGFR2 can induce preeclampsia-like symptoms.
    • ETK/BMX, a receptor tyrosine kinase, upregulates VEGF and interacts with VEGFR2, forming a signaling complex.

    Purpose of the Study:

    • To compare the activation status (phosphorylation levels) of VEGFR2 and ETK/BMX in kidney tissue from women with preeclampsia versus healthy pregnancies.

    Main Methods:

    • Analysis of renal tissue samples from six preeclamptic and six healthy pregnant women.
    • Utilized a RayBio® Phosphorylation Antibody Array to assess protein phosphorylation.

    Main Results:

    • Significantly lower levels of phosphorylated ETK/BMX were observed in preeclamptic women compared to healthy controls.
    • No significant difference in phosphorylated VEGFR2 levels was found between the two groups.

    Conclusions:

    • ETK/BMX appears to be a more critical mediator of VEGF function in the healthy pregnant kidney than VEGFR2.
    • Disruption of ETK/BMX-VEGF positive feedback signaling, or TNF-induced activation, may contribute to the development of preeclampsia.

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