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Elevated plasma endothelial microparticles in multiple sclerosis
1Department of Neurology, University of Miami, FL 33136, USA.
Objective:
To assess endothelial dysfunction in patients with MS and to investigate whether plasma from patients with MS induces endothelial cell dysfunction in vitro.
Background:
Endothelial cell dysfunction may contribute to the pathogenesis of MS. Elevations of soluble adhesion molecules intracellular adhesion molecule, vascular cell adhesion molecule, and platelet-endothelial cell adhesion molecule-1 (CD31) have been reported as markers of blood-brain barrier (BBB) damage in MS, but direct assay of endothelium has been difficult. Endothelial cells release microparticles < approximately 1.5 microm (EMP) during activation or apoptosis. The authors developed a flow cytometric assay of EMP and studied EMP as markers of endothelial damage in MS.
Methods:
Platelet-poor plasma (PPP) from 50 patients with MS (30 in exacerbation and 20 in remission) and 48 controls were labeled with fluorescein isothiocyanate (FITC)-conjugated anti-CD31 and anti-CD51 (vitronectin receptor) antibodies, and two classes of EMP (CD31+ and CD51+) were assayed by flow cytometry. For in vitro studies, patients' plasma was added to the microvascular endothelial cell (MVEC) culture and release of CD31+ and CD51+ EMP were measured in the supernatant.
Results:
Plasma from patients in exacerbation had 2.85-fold elevation of CD31+ EMP as compared with healthy controls, returning to near control value during remission. The CD31+ EMP concentration showed a positive association with gadolinium enhancement in patients with MS. In contrast, CD51+ EMP remained elevated in both exacerbation and remission. This suggests that CD31+ EMP is a marker of acute injury, whereas CD51+ EMP reflects chronic injury of endothelium. MS plasma induced release of both CD31+ and CD51+ EMP from MVEC culture in vitro.
Conclusion:
Endothelial dysfunction is evident during exacerbation of MS, evidenced by shedding of EMP expressing PECAM-1 (CD31). The in vitro data indicate contribution of one or more plasma factors in endothelial dysfunction of MS.
Insights
Endothelial dysfunction in multiple sclerosis (MS) patients is linked to elevated microparticle levels, particularly during exacerbations. MS plasma also induces endothelial cell dysfunction in vitro, suggesting plasma factors contribute to disease pathogenesis.
Area of Science:
- Neuroimmunology
- Vascular Biology
- Biomarker Discovery
Background:
- Endothelial cell dysfunction is implicated in the pathogenesis of multiple sclerosis (MS).
- Previous markers of blood-brain barrier damage in MS, like soluble adhesion molecules, have limitations.
- Endothelial microparticles (EMPs) are released during endothelial activation/apoptosis and can serve as markers of endothelial damage.
Purpose of the Study:
- To assess endothelial dysfunction in patients with MS.
- To investigate if plasma from MS patients induces endothelial cell dysfunction in vitro.
- To validate a novel flow cytometric assay for EMPs as markers of endothelial damage in MS.
Main Methods:
- Developed and utilized a flow cytometric assay to quantify two classes of EMPs (CD31+ and CD51+) in platelet-poor plasma from 50 MS patients and 48 controls.
- Assayed EMP levels in patients during MS exacerbation and remission.
- Investigated the effect of MS patient plasma on microvascular endothelial cell (MVEC) cultures in vitro, measuring EMP release.
Main Results:
- Patients with MS in exacerbation showed a 2.85-fold increase in CD31+ EMPs compared to controls, which normalized during remission, indicating CD31+ EMPs as markers of acute endothelial injury.
- CD51+ EMPs remained elevated in both exacerbation and remission phases, suggesting they reflect chronic endothelial injury.
- MS patient plasma significantly induced the release of both CD31+ and CD51+ EMPs from MVEC cultures in vitro.
Conclusions:
- Endothelial dysfunction, marked by the shedding of PECAM-1 (CD31)-expressing EMPs, is evident during MS exacerbations.
- The in vitro findings suggest that plasma-derived factors contribute to endothelial dysfunction in MS.
- CD31+ EMPs serve as a marker for acute endothelial injury, while CD51+ EMPs indicate chronic injury in MS.
