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Related Experiment Video

Updated: Mar 2, 2026

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

Published on: November 26, 2018

Age Increases Monocyte Adhesion on Collagen.

Samira Khalaji¹, Lisa Zondler², Fenneke KleinJan¹

¹Institute for Experimental Physics, Ulm University, Ulm, Germany.

Scientific Reports

|May 18, 2017

Summary

This summary is machine-generated.

Monocyte adhesion to collagen increases with age due to heightened integrin activation, raising the risk of arteriosclerotic plaques. This study reveals age-related changes in monocyte behavior contributing to atherosclerosis development.

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Last Updated: Mar 2, 2026

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

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Published on: November 26, 2018

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

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Published on: October 17, 2017

Area of Science:

Cardiovascular Research
Immunology
Aging Research

Background:

Monocyte adhesion to arterial micro-injuries, exposing collagen, initiates atherosclerotic lesion development.
Age is a significant risk factor for atherosclerosis, but the underlying cellular mechanisms remain incompletely understood.

Purpose of the Study:

To investigate the influence of age on monocyte adhesion to collagen under flow conditions.
To determine if age-related changes in monocyte-collagen interactions contribute to increased arteriosclerotic lesion susceptibility.

Main Methods:

Studied adhesion and rolling of monocytes from young and old individuals on collagen type I surfaces under shear flow.
Utilized lipopolysaccharide stimulation and integrin blocking (αx) to analyze monocyte-collagen interactions.
Assessed gene expression of integrins αx and β2 and evaluated integrin activation.

Main Results:

Firm monocyte adhesion to collagen type I was elevated in older individuals.
Adhesion was primarily mediated by the integrin αxβ2, with no significant age-dependent difference in integrin gene expression.
Altered basal integrin activation, not gene expression, was identified as the cause of increased adhesion in older individuals.

Conclusions:

Increased basal integrin activation in monocytes from older individuals enhances their adhesion to collagen.
This age-related increase in monocyte adhesion contributes to a higher risk of developing arteriosclerotic plaques.