Tiny pieces of damaged endothelial cells, aptly called “microparticles” due to their size, can be generated in patients with systemic sclerosis (SSc). These cell particulates are created from a variety of processes, but are often the result of inflammation or shear stress from blood flow in narrowed arteries. Since pulmonary arterial hypertension (PAH) is a common co-morbidity in SSc patients, cell microparticles in these patients might be the result of cellular damage.
To be sure of the origin of cell microparticles in SSc patients, a team of researchers from Copenhagen University Hospital conducted a study to analyze cell microparticles from patient plasma, entitled “Cross-Sectional Study of Soluble Selectins, Fractions of Circulating Microparticles and Their Relationship to Lung and Skin Involvement in Systemic Sclerosis.” It was published in BMC Musculoskeletal Disorders.
Using a specialized technique called flow cytometry, the researchers analyzed the cell microparticles held within patients’ plasma. The researchers applied antibodies that are targeted against specific proteins that are present in specific cells types to patient serum to determine the origins of the microparticles. Annexin V, CD146, CD45, and CD42a were used as the antibodies. CD146-positive indicates an endothelial cell, CD45 indicates a leukocyte, and CD42a indicates a platelet. Researchers are still understanding annexin V proteins.
The researchers determined that microparticles were derived from these three cell types. Those microparticles that did not display any annexin V binding were inversely correlated to lung function if the microparticles were from endothelial cells or leukocytes, but not platelets. Annexin V-positive microparticles held no information regarding disease severity.
In addition to determining the origin of cell microparticles, the researchers were interested in knowing if the markers on the microparticle surfaces correlated with disease characteristics or severity. They found no correlation between quantity of microparticles or soluble selectins with modified Rodnan skin score (a test used to evaluate SSc severity) in any of the patients. Looking at the difference between features of lcSSc versus dcSSc patients, the researchers noted that the dcSSc patients had a significantly lower vital capacity (FVC) in the lungs. This change was accompanied by an increase in soluble E-selectin. Interestingly, there was no difference between dcSSc and lcSSc in terms of diffusing capacity (DLCO). The researchers found that DLCO directly correlated with P-selectin.
Altogether, there seems to be more information held within the characteristics of cell microparticles than selectins regarding SSc status. Investigating these microparticles further may help to better understand the pathogenesis of disease and enhance disease activity monitoring in patients with SSc.