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Intima modifier locus 2 controls endothelial cell activation and vascular permeability.

Elaine M Smolock1, Ryan M Burke1, Chenjing Wang2

  • 1Department of Medicine and Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York;

Physiological Genomics
|July 3, 2014
PubMed
Summary

The Intima modifier 2 (Im2) locus regulates leukocyte infiltration into blood vessels by increasing endothelial cell inflammation and permeability, not by altering circulating immune cells. This finding reveals genetic mechanisms controlling vascular intima formation.

Keywords:
C3Heb/FeSJLcongenicsendothelial cellinflammationpermeability

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Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Genetics

Background:

  • Carotid intima formation is a key risk factor for cardiovascular disease.
  • Genetic variations influence susceptibility to immune and vascular traits, as seen in C3H/FeJ and SJL/J mouse strains.
  • The Intima modifier 2 (Im2) locus on chromosome 11 has been implicated in regulating leukocyte infiltration.

Purpose of the Study:

  • To investigate whether the Im2 locus mediates inflammation through changes in circulating immune cells or activation of vascular wall cells.
  • To analyze the role of the Im2 locus in endothelial cell inflammation and permeability in genetically pure mice.

Main Methods:

  • Congenic mouse strains (C3H/F.SJL.11.1) were used to study the Im2 locus.
  • Complete blood counts were performed to assess circulating monocytes.
  • Aortic vascular cell adhesion molecule-1 (VCAM-1) expression, endothelial cell size, and vascular permeability were analyzed using immunostaining and other techniques.
  • RNA sequencing and pathway analyses were conducted to identify candidate genes.

Main Results:

  • No significant differences in circulating monocytes were observed between strains.
  • Aortic VCAM-1 protein levels and endothelial cell VCAM-1 expression were significantly increased in SJL and C3H/F.SJL.11.1 mice compared to C3H/F mice.
  • Endothelial cell size decreased, and vascular permeability increased in C3H/F.SJL.11.1 mice, particularly in regions of disturbed flow.
  • RNA sequencing identified candidate genes within the Im2 locus regulating vascular wall inflammation and permeability.

Conclusions:

  • The Im2 locus regulates leukocyte infiltration primarily through endothelial cell inflammation and increased vascular permeability.
  • These findings highlight genetic mechanisms controlling vascular intima formation in response to injury.
  • The study provides insights into candidate genes that mediate vascular wall inflammation and permeability.