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Designing Effective Multi-Target Drugs and Identifying Biomarkers in Recurrent Pregnancy Loss (RPL) Using In Vivo, In

Andrés Alexis Ramírez-Coronel1,2,3,4, Amirabbas Rostami5, Laith A Younus6

  • 1Epidemiology and Biostatistics Group, Research Group in Educational Statistics, National University of Education (UNAE), Azogues 030102, Ecuador.

Biomedicines
|March 29, 2023
PubMed
Summary
This summary is machine-generated.

Polo-like kinase 1 (PLK1) plays a protective role in recurrent pregnancy loss (RPL). Decreased PLK1 expression in RPL patients disrupts mitochondrial function and promotes apoptosis, suggesting PLK1 as a therapeutic target.

Keywords:
NF-κB signaling pathwayRPLbiomarkershub geneshub high traffic genepolo-like kinase 1recurrent pregnancy loss

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Area of Science:

  • Reproductive Biology and Medicine
  • Molecular and Cellular Biology
  • Genetics and Genomics

Background:

  • Recurrent pregnancy loss (RPL) affects approximately 5% of women, with its molecular mechanisms remaining largely unclear.
  • Understanding the underlying pathology of RPL is crucial for developing effective diagnostic and therapeutic strategies.

Purpose of the Study:

  • To investigate the role of polo-like kinase 1 (PLK1) in the pathogenesis of recurrent pregnancy loss (RPL).
  • To identify key molecular players and pathways involved in RPL using network analysis and clinical samples.

Main Methods:

  • Construction of a regulatory network for RPL using GEO datasets to identify hub genes.
  • Analysis of PLK1 expression in chorionic villi from women with RPL versus healthy pregnancies.
  • Validation using in vitro (cell lines) and in vivo (mouse models) studies, including PLK1 knockdown/overexpression and inhibitor treatment.
  • Evaluation of apoptosis, mitochondrial function, and signaling pathways (NF-κB, Foxo, PI3K/AKT).

Main Results:

  • PLK1 was identified as a hub gene in the RPL network. Significantly decreased PLK1 expression was observed in chorionic villi of RPL patients compared to controls.
  • In vitro, PLK1 knockdown led to increased apoptosis and NF-κB signaling, while reducing cell invasion, migration, and proliferation.
  • In vivo, PLK1 suppression impaired mitochondrial function and chorionic villi development.
  • The PLK1/TRAF2/NF-κB axis was identified as a critical regulator of mitochondrial dynamics and apoptosis in RPL.

Conclusions:

  • PLK1 exhibits a protective role in recurrent pregnancy loss by maintaining mitochondrial function and suppressing apoptosis.
  • The PLK1/TRAF2/NF-κB signaling pathway is a key player in RPL-induced chorionic villi dysfunction.
  • PLK1 and its associated axis represent a potential therapeutic target for managing recurrent pregnancy loss.