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Monocyte-platelet complexes on CD14/CD16 monocyte subsets: relationship with ApoA-I levels. A preliminary study
Karim Zouaoui Boudjeltia1, Dany Brohee, Pietrina Piro
1Laboratoire de Médecine Expérimentale (ULB 222 Unit), ISPPC Hopital André Vesale, Montigny-Le-Tilleul, Belgium. karim.zouaoui@chu-charleroi.be
Insights
High-density lipoprotein (HDL) and apolipoprotein A-I (ApoA-I) levels are negatively correlated with monocyte-platelet complexes (MPCs), suggesting a role in reducing atherogenesis. The G2 monocyte subset shows higher potential for extravasation, indicating increased involvement in atherosclerotic lesion development.
Area of Science:
- Cardiovascular Biology
- Immunology
- Lipid Metabolism
Background:
- Monocyte adhesion and extravasation are critical in atherogenesis.
- L-selectin (CD62-L) on monocytes and platelet interactions are key.
- High-density lipoprotein (HDL) and apolipoprotein A-I (ApoA-I) exhibit anti-inflammatory effects on monocytes.
Purpose of the Study:
- To investigate the relationship between monocyte-platelet complexes (MPCs), monocyte subsets, and serum ApoA-I/HDL levels in vivo.
- To characterize monocyte subsets involved in MPC formation.
- To explore the potential extravasation capacity of different monocyte subsets.
Main Methods:
- Flow cytometry was used to quantify MPCs (CD42b+ monocytes) in 16 volunteers.
- Monocytes were classified into four subsets (G1-G4) based on CD14 and CD16 expression.
- Serum HDL and ApoA-I levels were measured using standard laboratory methods.
Main Results:
- MPC percentage varied significantly across monocyte subsets (G1=8.1%, G2=21.2%, G3=18%, G4=22.3%; P<.001).
- MPC percentage negatively correlated with ApoA-I levels (R=-0.71, P=.001), particularly in G1 and G2 subsets.
- The G2 subset exhibited the highest MPC percentage and potential for extravasation, linked to CD62-L expression.
Conclusions:
- Serum ApoA-I/HDL levels are inversely associated with MPCs, suggesting a protective role against atherogenesis.
- The G2 monocyte subset, characterized by high CD14/CD16 expression and platelet coating, may be more implicated in atherosclerotic lesion development.
- HDL/ApoA-I does not directly interact with the platelet marker CD42b.
Abstract:
The adhesion of the monocytes to the endothelium and their extravasation into the intima are key steps in atherogenesis. Studies showed the essential role of L-selectin (CD62-L), expressed by the monocytes, and the platelets by forming complexes with monocytes. The delipided apolipoprotein (Apo) A or high-density lipoprotein (HDL) has antiinflammatory effects on monocytes and can bind platelets (monocyte-platelet complexes [MPCs]). The aim of this study was to identify a possible relationship between the MPCs, the monocyte subset, and ApoA-I/HDL serum levels in vivo. Platelet-monocyte complexes were estimated by flow cytometry in 16 volunteers. Monocyte-platelet interaction was characterized by the percentage of monocytes coexpressing the constitutive platelet marker, glycocalicin gpIb-alpha (CD42b; CD42b+monocytes in %, MPC%). Monocytes were divided into four subsets based on lipopolysaccharide receptor (CD14) and FcgammaIII receptor (CD16) expression (CD14++/CD16-, G1; CD14++/CD16+, G2; CD14+/CD16-, G3; and CD14+/CD16+, G4). HDL and ApoA-I levels were measured by routine laboratory techniques. MPC% in the different subsets were G1=8.1+/-3.4%, G2=21.2+/-14%, G3=18+/-12.6%, and G4=22.3+/-14.3% (analysis of variance: P<.001). MPC% in the entire monocyte population was negatively correlated to ApoA-I (R=-0.71, P=.001). The relationship between ApoA-I and MPC% was found mainly in the subsets G1 (R=-0.67, P=.001) and G2 (R=-0.61, P=.01). MPC% was not correlated with any other lipids or lipoprotein or high-sensitivity C-reactive protein. When whole blood was incubated with HDL/ApoA-I, no modification of platelet CD42b fluorescence was observed, indicating that there is no direct interaction between the HDL/ApoA-I and the CD42b fluorescence. Among the monocytes, the G2 subset appeared to have the highest extravasation potential. Indeed, we previously showed that those cells overexpressed CD62-L, and we observed in this work that they were coated with platelets more than the G1 cells. The G2 subset could be more directly involved in the development of atherosclerotic lesions.
