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Updated: Jun 4, 2026
Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
Published on: November 26, 2018
VEGF-A-induced chemotaxis of CD16+ monocytes is decreased secondary to lower VEGFR-1 expression
Frauke S Czepluch1, Servé Olieslagers, Ruud van Hulten
1Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, The Netherlands.
Insights
Monocyte subsets CD14++CD16- (CD16-mo) and CD14+CD16+ (CD16+mo) show distinct functions. CD16+mo exhibit reduced migration and adhesion, potentially due to lower VEGFR-1 expression, but possess greater oxidative resistance.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Monocyte recruitment is key in vascular repair, arteriogenesis, and atherogenesis.
- Two human monocyte subsets, CD14++CD16- (CD16-mo) and CD14+CD16+ (CD16+mo), differ in surface marker expression.
- Understanding functional differences between these subsets is crucial for vascular disease research.
Purpose of the Study:
- To investigate and compare the functional properties of CD16-mo and CD16+mo.
- To elucidate the roles of these monocyte subsets in vascular processes.
- To identify potential differences in their response to angiogenic factors and oxidative stress.
Main Methods:
- Isolation of CD16-mo and CD16+mo from human blood via immunological selection.
- Assessment of monocyte chemokinesis, chemotaxis, and adhesion.
- Analysis of Vascular-Endothelial Growth Factor (VEGF) receptor expression (VEGFR-1).
- Investigation of reactive oxygen species (ROS) generation and antioxidant enzyme expression (manganese superoxide dismutase).
Main Results:
- CD16+mo displayed significantly decreased chemokinesis and adhesion compared to CD16-mo.
- Chemotaxis of CD16+mo towards VEGF-A and PlGF-1 was reduced, correlated with lower VEGFR-1 expression.
- CD16+mo showed less spontaneous ROS production and higher levels of manganese superoxide dismutase, indicating greater oxidative resistance.
Conclusions:
- Novel functional disparities exist between CD16-mo and CD16+mo.
- These differences, including migration, adhesion, and oxidative stress response, suggest distinct roles in vascular repair, arteriogenesis, and atherogenesis.
- Further research into these monocyte subsets could offer insights into therapeutic strategies for vascular diseases.
Background:
Monocyte recruitment into the vessel wall is a crucial initial step in vascular repair, arteriogenesis and atherogenesis. Two distinct human monocyte subpopulations can be classified according to their CD14/16 surface expression, namely CD14++CD16-monocytes (CD16-mo) and CD14+CD16+ monocytes (CD16+mo). We investigated different functional properties of the two monocyte subsets.
Methods:
CD16-/CD16+mo were isolated from human blood by an immunological selection. We assessed monocyte chemokinesis, chemotaxis, adhesion and Vascular-Endothelial Growth Factor (VEGF) receptor expression. Furthermore, generation of reactive oxygen species (ROS) as well as expression of antioxidant enzymes was investigated.
Results:
Chemokinesis of CD16+mo was decreased compared to CD16-mo (p<0.01). Likewise, adhesion capacity of CD16+mo was weaker (p<0.05). CD16+mo chemotaxis towards the angiogenic ligands vascular endothelial growth factor-A (VEGF-A) and placenta growth factor-1 (PlGF-1) was reduced compared to CD16-mo. VEGFR-1 is the receptor for VEGF-A and PlGF-1 on monocytes. VEGFR-1 protein expression was lower in CD16+mo than in CD16-mo (p<0.05). The impaired VEGF-A- and PlGF-1-induced CD16+mo chemotaxis might therefore be attributed to the reduced VEGFR-1 expression. CD16+mo exhibited less spontaneous ROS production than CD16-mo. Additionally, the antioxidant enzyme manganese superoxide dismutase was expressed at higher levels in CD16+mo (p<0.05); this might partly explain the higher oxidative resistance of CD16+mo.
Conclusion:
These novel functional differences between CD16-mo and CD16+mo may predict different functional roles of both monocyte subsets in vascular repair, arteriogenesis and atherogenesis.
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