Biomolecules (Sep 2024)

Placental Tissue Calcification and Its Molecular Pathways in Female Patients with Late-Onset Preeclampsia

  • Miguel A. Ortega,
  • Tatiana Pekarek,
  • Diego De Leon-Oliva,
  • Diego Liviu Boaru,
  • Oscar Fraile-Martinez,
  • Cielo García-Montero,
  • Julia Bujan,
  • Leonel Pekarek,
  • Silvestra Barrena-Blázquez,
  • Raquel Gragera,
  • Patrocinio Rodríguez-Benitez,
  • Mauricio Hernández-Fernández,
  • Laura López-González,
  • Raul Díaz-Pedrero,
  • Ángel Asúnsolo,
  • Melchor Álvarez-Mon,
  • Natalio García-Honduvilla,
  • Miguel A. Saez,
  • Juan A. De León-Luis,
  • Coral Bravo

DOI
https://doi.org/10.3390/biom14101237
Journal volume & issue
Vol. 14, no. 10
p. 1237

Abstract

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Preeclampsia (PE) is a complex multisystem disease characterized by hypertension of sudden onset (>20 weeks’ gestation) coupled with the presence of at least one additional complication, such as proteinuria, maternal organ dysfunction, or uteroplacental dysfunction. Hypertensive states during pregnancy carry life-threatening risks for both mother and baby. The pathogenesis of PE develops due to a dysfunctional placenta with aberrant architecture that releases factors contributing to endothelial dysfunction, an antiangiogenic state, increased oxidative stress, and maternal inflammatory responses. Previous studies have shown a correlation between grade 3 placental calcifications and an elevated risk of developing PE at term. However, little is known about the molecular pathways leading to placental calcification. In this work, we studied the gene and protein expression of c-Jun N-terminal kinase (JNK), Runt-related transcription factor 2 (RUNX2), osteocalcin (OSC), osteopontin (OSP), pigment epithelium-derived factor (PEDF), MSX-2/HOX8, SOX-9, WNT-1, and β-catenin in placental tissue from women with late-onset PE (LO-PE). In addition, we employed von Kossa staining to detect mineral deposits in placental tissues. Our results show a significant increase of all these components in placentas from women with LO-PE. Therefore, our study suggests that LO-PE may be associated with the activation of molecular pathways of placental calcification. These results could be the starting point for future research to describe the molecular mechanisms that promote placental calcification in PE and the development of therapeutic strategies directed against it.

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