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Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries
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Mononuclear Cells Negatively Regulate Endothelial Ca2+ Signaling.

Aishwarya Rengarajan1, Jason L Austin1, Aleksandar K Stanic1

  • 1Department of Obstetrics & Gynecology, University of Wisconsin-Madison, School of Medicine and Public Health, Perinatal Research Laboratories, 7E UnityPoint Health-Meriter Hospital, 202 South Park St, Madison, WI, 53715, USA.

Reproductive Sciences (Thousand Oaks, Calif.)
|January 30, 2023
PubMed
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Immune cells, specifically peripheral blood mononuclear cells (PBMCs), impair endothelial calcium signaling in blood vessels. This interaction, mediated by secreted proteins, may contribute to pregnancy complications like preeclampsia.

Keywords:
Calcium signalingEndothelial cellsMononuclear cellsPregnancy

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Area of Science:

  • Cardiovascular Biology
  • Reproductive Immunology
  • Cellular Physiology

Background:

  • Endothelial calcium (Ca2+) signaling is crucial for pregnancy-associated vasodilation in the utero-placenta.
  • Elevated inflammatory cytokines in pregnancy complications negatively impact endothelial Ca2+ signaling and nitric oxide production.
  • The direct impact of immune cell engagement on endothelial Ca2+ signaling and function remains largely unknown.

Purpose of the Study:

  • To investigate the effects of peripheral blood mononuclear cells (PBMCs) on agonist-stimulated Ca2+ signaling in human umbilical vein endothelial cells (HUVECs).
  • To model immune-endothelial interactions relevant to pregnancy complications.

Main Methods:

  • Short-term co-culture of HUVECs with PBMCs or specific immune cell lines (THP-1, NKL, Jurkat).
  • Measurement of ATP-stimulated Ca2+ signaling in HUVECs.
  • Assessment of Ca2+ signaling rescue by inhibiting protein transport in PBMCs.

Main Results:

  • PBMCs significantly decreased ATP-stimulated Ca2+ signaling in HUVECs.
  • Activated PBMCs and specific immune cell types (monocytes, NK cells, T-cells) exacerbated this decrease.
  • Inhibiting protein transport in PBMCs restored endothelial Ca2+ signaling, indicating a role for secreted factors.

Conclusions:

  • Secreted proteins from PBMCs mediate the observed changes in endothelial Ca2+ signaling.
  • This immune-endothelial interaction model may represent mechanisms underlying endothelial dysfunction in preeclampsia.
  • Understanding these interactions is vital for addressing vascular complications in pregnancy.