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Src kinase partially mediates cytokine-induced endothelial dysfunction.

Amanda K Mauro1, Luca Clemente1, Nauman Khurshid2

  • 1Perinatal Research Laboratories, Department of Obstetrics & Gynecology, University of Wisconsin - Madison, School Medicine and Public Health, Madison, WI 53715, USA.

Pregnancy Hypertension
|October 21, 2023
PubMed
Summary
This summary is machine-generated.

Src kinase partially mediates endothelial dysfunction in preeclampsia by affecting calcium signaling and monolayer integrity. Inhibiting Src kinase protected against insults, suggesting a therapeutic target for endothelial-based treatments.

Keywords:
CytokineEndothelialGrowth factorHUVECPreeclampsiaSrc kinase

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Area of Science:

  • Vascular Biology
  • Cell Signaling
  • Preeclampsia Pathophysiology

Background:

  • Endothelial dysfunction is central to preeclampsia (PE), contributing to organ damage.
  • Growth factors and cytokines dysregulate endothelial function in PE, impacting calcium (Ca2+) signaling and barrier integrity.
  • Delivery is the only PE treatment, necessitating novel endothelial-based therapeutic strategies.

Purpose of the Study:

  • To investigate the role of Src kinase in mediating endothelial dysfunction induced by growth factors and cytokines in preeclampsia.
  • To determine if Src kinase inhibition can reverse endothelial dysfunction in a cellular model of PE.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were exposed to growth factors or cytokines.
  • Calcium (Ca2+) imaging and Electrical Cell Impedance Sensing (ECIS) were used to assess endothelial function.
  • Kinase inhibitors (Src inhibitor PP2, MEK/ERK inhibitor U0126) were employed to elucidate signaling pathways.

Main Results:

  • Src kinase inhibition protected HUVECs from Ca2+ signaling disruptions caused by VEGF165, bFGF, PlGF, TNFα, and IL-1β.
  • Src inhibition also preserved endothelial monolayer resistance against TNFα-induced insult.
  • MEK/ERK inhibition did not protect against growth factor-mediated endothelial dysfunction.

Conclusions:

  • Cytokine and growth factor-stimulated Src kinase partially promotes endothelial dysfunction in HUVECs.
  • Targeting Src kinase represents a potential therapeutic strategy for preeclampsia-related endothelial dysfunction.