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Updated: May 9, 2026
05:31
Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
Published on: January 26, 2024
Impaired Midkine/Treg Signaling Contributes to Pathogenesis of Preeclampsia
Liqun Lou1,2,3, Ye Chen3, Shengyi Gu2
1Department of Obstetrics, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China (L.L., S.Q., C.Z., W.L., X.H.).
Hypertension (Dallas, Tex. : 1979)
|May 8, 2026
Summary
Restoring regulatory T cells (Tregs) improves trophoblast function to combat early-onset preeclampsia. Midkine (MDK) enhances this therapy by upregulating latency-associated peptide (LAP) on Tregs, boosting efficacy.
Area of Science:
- Immunology
- Reproductive Biology
- Maternal-Fetal Medicine
Background:
- Early-onset preeclampsia involves immune dysregulation and impaired trophoblast invasion, often linked to reduced regulatory T cells (Tregs).
- The exact role of Treg-trophoblast interactions in preeclampsia pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the therapeutic potential of regulatory T cells (Tregs) in mitigating early-onset preeclampsia.
- To explore the role of midkine (MDK) in enhancing Treg-based therapies for preeclampsia.
Main Methods:
- Established preeclampsia-like mouse models using nitric oxide or MDK/PI3K/Akt inhibitors.
- Adoptively transferred mouse Tregs into disease models and utilized in vitro trophoblast-Treg co-culture systems.
- Analyzed placental tissues, measured MDK levels, and assessed Treg function and signaling pathways.
Main Results:
- Reduced Treg numbers were observed in placentas from early-onset preeclampsia patients.
- Adoptive Treg transfer enhanced trophoblast invasion and proliferation via the TβR1/Smad3 pathway, alleviating preeclampsia-like symptoms.
- Maternal MDK levels inversely correlated with disease severity, and MDK synergized with Treg transfer by upregulating Treg LAP expression.
Conclusions:
- Restoring Tregs enhances trophoblast function, ameliorating preeclampsia-like syndromes.
- Midkine (MDK) acts as a key mediator, enhancing therapeutic efficacy by upregulating latency-associated peptide (LAP) on Tregs for early-onset preeclampsia treatment.
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