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HIV-1 envelope glycoprotein 120 increases intercellular adhesion molecule-1 expression by human endothelial cells
Zeguang Ren1, Qizhi Yao, Changyi Chen
1Department of Surgery, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Summary
HIV-1 infection increases intercellular adhesion molecule-1 (ICAM-1) in endothelial cells via gp120. This elevates monocyte adhesion, suggesting a key mechanism in HIV-1 pathogenesis and vascular complications.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Human immunodeficiency virus type 1 (HIV-1) infection is linked to neurological and vascular issues.
- The precise mechanisms behind these complications remain largely unelucidated.
Purpose of the Study:
- To investigate the impact of HIV-1 envelope glycoprotein 120 (gp120) on endothelial cell adhesion molecule expression.
- To determine if gp120 influences intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression.
Main Methods:
- Assessed mRNA and protein levels of ICAM-1 and VCAM-1 in endothelial cells exposed to gp120.
- Utilized blocking experiments with anti-gp120 monoclonal antibodies.
- Measured the adherence of THP-1 monocytic cells to gp120-treated endothelial monolayers.
Main Results:
- Both soluble and membrane-bound gp120 significantly upregulated ICAM-1 at mRNA and protein levels.
- gp120 did not affect VCAM-1 or E-selectin expression.
- gp120-induced ICAM-1 expression and subsequent THP-1 cell adhesion were blocked by anti-gp120 and anti-ICAM antibodies.
Conclusions:
- HIV-1 gp120 elevates endothelial ICAM-1 expression.
- This upregulation enhances monocyte adhesion to endothelial cells.
- gp120-mediated ICAM-1 expression is a potential mechanism contributing to HIV-1 pathogenesis and vascular complications.