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Impaired Vitamin D Signaling in Endothelial Cell Leads to an Enhanced Leukocyte-Endothelium Interplay: Implications

Milica Bozic1, Ángeles Álvarez2, Carmen de Pablo2

  • 1Nephrology Research Department, IRB Lleida, Lleida, Spain.

Plos One
|September 1, 2015
PubMed

Insights

Low vitamin D receptor (VDR) levels in endothelial cells promote inflammation and increase leukocyte adhesion, contributing to atherosclerosis development. Restoring VDR signaling is crucial for preventing cardiovascular damage.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Immunology

Background:

  • Endothelial cell activation drives atherosclerosis initiation and progression.
  • Vitamin D deficiency is linked to increased cardiovascular damage.
  • The role of basal vitamin D receptor (VDR) levels in early atherosclerosis is unclear.

Purpose of the Study:

  • To investigate the role of basal VDR levels in endothelial cells on leukocyte recruitment.
  • To assess VDR's impact on endothelial cell adhesion molecule expression.
  • To understand VDR's role in early atherosclerosis development.

Main Methods:

  • VDR knockdown in endothelial cells (shVDR) was performed.
  • Leukocyte-endothelial cell interactions were analyzed in vitro.
  • NF-κB pathway activation was assessed.
  • Atherosclerotic lesion development was studied in VDR-deficient mice (apoE-/-VDR-/-).

Main Results:

  • VDR knockdown increased VCAM-1, ICAM-1, and IL-6 expression.
  • Reduced PBMC rolling velocity and increased adhesion were observed in shVDR cells.
  • VDR deficiency in mice led to larger aortic lesions and higher macrophage content.
  • NF-κB pathway activation mediated VDR knockdown-induced endothelial activation.

Conclusions:

  • Basal VDR signaling in endothelial cells limits inflammation and leukocyte recruitment.
  • VDR deficiency promotes endothelial activation and exacerbates atherosclerosis.
  • Endothelial VDR is a key factor in preventing early atherosclerotic lesion formation.

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