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Updated: Jun 8, 2026

In vivo Measurement of the Mouse Pulmonary Endothelial Surface Layer
08:55

In vivo Measurement of the Mouse Pulmonary Endothelial Surface Layer

Published on: February 22, 2013

Gene expression of adhesion molecules in pulmonary and hepatic microvascular endothelial cells during sepsis

Rongqian Wu1, Yingxin Xu, Xuhua Song

  • 1Institute of Surgical Research, General Hospital of PLA, Beijing 100853, China. wurq@yahoo.com

Chinese Journal of Traumatology = Zhonghua Chuang Shang Za Zhi
|May 30, 2002
PubMed
Abstract

Insights

Sepsis upregulates adhesion molecule gene expression in mouse lung and liver endothelial cells, contributing to leukocyte migration and organ damage. This highlights the role of endothelial cell heterogeneity in sepsis vulnerability.

Area of Science:

  • Endothelial cell biology
  • Sepsis research
  • Molecular mechanisms of inflammation

Background:

  • Sepsis involves complex inflammatory responses impacting multiple organs.
  • Endothelial cells play a crucial role in regulating leukocyte trafficking during inflammation.

Purpose of the Study:

  • To investigate the gene expression of adhesion molecules in pulmonary and hepatic microvascular endothelial cells during murine sepsis.
  • To correlate adhesion molecule expression with myeloperoxidase activity as an indicator of neutrophil infiltration.

Main Methods:

  • Murine model of sepsis induced by cecal ligation and puncture (CLP).
  • Isolation of pulmonary and hepatic microvascular endothelial cells at early (3 hours) and late (12 hours) sepsis.
  • Assessment of adhesion molecule gene expression (E-selectin, ICAM-1, VCAM-1) via RT-PCR.
  • Measurement of myeloperoxidase (MPO) activity in tissue homogenates.

Main Results:

  • Marked increase in E-selectin mRNA at 3 hours post-CLP, returning to baseline by 12 hours.
  • Sustained increase in intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) mRNA levels throughout early and late sepsis.
  • Differential VCAM-1 expression patterns observed between pulmonary and hepatic endothelial cells.
  • Increased MPO activity in both tissues at 3 hours, with a significant decline but remaining elevated at 12 hours post-CLP.

Conclusions:

  • Up-regulation of adhesion molecule gene expression in endothelial cells is critical for leukocyte recruitment and subsequent organ damage in sepsis.
  • Organ-specific heterogeneity in endothelial cell responses contributes to differential vulnerability during sepsis.
  • Further investigation into endothelial cell heterogeneity is warranted to understand organ-specific sepsis pathogenesis.

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