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FABP4 Downregulated by FOS Alleviates Palmitic Acid-induced Endothelial Cell Dysfunction Via Inactivating ERK/STAT-1

Mengting Ruan1, Jin Zhang2

  • 1Department of Obstetrics, Zhuji People's Hospital of Zhejiang Province, Zhuji, Zhejiang, P.R. China.

Cell Biochemistry and Biophysics
|July 28, 2025
PubMed

Insights

Fatty acid-binding protein 4 (FABP4) is elevated in preeclampsia (PE). FABP4 interference protects against palmitic acid-induced endothelial cell dysfunction by inhibiting the ERK/STAT-1 pathway, potentially mediated by FOS.

Area of Science:

  • Reproductive Biology
  • Molecular Medicine
  • Cellular Biology

Background:

  • Preeclampsia (PE) is a serious pregnancy complication characterized by hypertension and organ damage.
  • The underlying mechanisms of PE pathogenesis remain incompletely understood, necessitating further investigation into key molecular players.
  • Fatty acid-binding protein 4 (FABP4) has been implicated in metabolic disorders, but its specific role in PE is unclear.

Purpose of the Study:

  • To elucidate the role of FABP4 in the pathogenesis of preeclampsia (PE).
  • To investigate the underlying molecular mechanisms by which FABP4 influences endothelial cell function in PE.
  • To explore the potential involvement of the FOS protein in regulating FABP4 activity and its downstream signaling.

Main Methods:

  • Quantification of FABP4 expression in blood and placental tissues from PE patients and controls using RT-qPCR.
  • In vitro studies using human umbilical vein endothelial cells (HUVECs) treated with palmitic acid (PA) to mimic PE conditions.
  • Manipulation of FABP4 and FOS expression via transfection (sh-FABP4, sh-FOS, Ov-FOS) and assessment of cell viability, apoptosis (TUNEL assay), migration, invasion (wound healing, Transwell assays), and angiogenesis (tube formation assay).
  • Analysis of apoptosis-related proteins and the ERK/STAT-1 signaling pathway via Western blotting.
  • Luciferase reporter and ChIP assays to determine FABP4 promoter activity and FOS binding to FABP4.

Main Results:

  • FABP4 expression was significantly increased in the blood and placental tissues of PE patients and in PA-treated HUVECs.
  • Interference with FABP4 expression reduced apoptosis and enhanced migration, invasion, and angiogenesis in PA-induced HUVECs by inactivating the ERK/STAT-1 signaling pathway.
  • FOS was found to reduce FABP4 activity and inhibit the FABP4/ERK/STAT-1 signaling pathway, suggesting a protective role.

Conclusions:

  • FABP4 plays a crucial role in the pathogenesis of preeclampsia by promoting endothelial cell dysfunction.
  • FABP4 exacerbates PA-induced endothelial cell injury via activation of the ERK/STAT-1 signaling pathway.
  • FOS may protect against PA-induced endothelial cell dysfunction by inhibiting the FABP4/ERK/STAT-1 pathway, highlighting a potential therapeutic target for PE.

Keywords:
ERK/STAT-1Endothelial cell dysfunctionFABP4FOSPalmitic acidPreeclampsia

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