Related Experiment Video
Updated: Jan 29, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
Published on: June 16, 2020
Microparticles in systemic sclerosis: Potential pro-inflammatory mediators and pulmonary hypertension biomarkers
Matthew R Lammi1,2, Lesley Ann Saketkoo2,3, Samuel C Okpechi4,5
1Section of Pulmonary/Critical Care and Allergy Immunology, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Background And Objective:
Endothelial microparticles (EMP) are submicron vesicles released from endothelial cells. We aimed to determine the utility of EMP as biomarkers of pulmonary arterial hypertension (PAH) in systemic sclerosis (SSc) patients and the pathogenic role of microparticles (MP) in vascular inflammation.
Methods:
Levels of EMP (CD144+, CD31+, CD62E+ and CD143+) were compared between three groups (10 SSc patients with PAH, 10 SSc patients without pulmonary hypertension (no-PH) and 10 healthy age- and sex-matched controls). Human pulmonary artery endothelial cells (HPAEC) were exposed in vitro to MP obtained from SSc patients or healthy controls, and levels of cytokines and inflammatory adhesion molecules were compared.
Results:
CD144+ EMP were significantly higher in the SSc-PAH group compared to either the SSc-no PH or healthy controls (diagnostic accuracy 80%, P = 0.02). Compared to controls, SSc patients had higher CD31+/CD62E+ ratios, indicating larger contributions of apoptosis to EMP release (P = 0.04). Patients with limited SSc had significantly higher levels of CD143+ EMP compared to those with diffuse subtype (P = 0.008). When HPAEC were exposed to MP from SSc patients, there was a significant increase in inflammatory cytokines and adhesion molecules. Interestingly, exposure to healthy control MP caused a reduction in inflammatory markers.
Conclusion:
EMP (particularly CD144+) are promising biomarkers of PAH in SSc but require further study. MP isolated from SSc patients induced an increase in endothelial cell inflammation and may be an important pathogenic factor in SSc.
Insights
Endothelial microparticles (EMP) show promise as biomarkers for pulmonary arterial hypertension (PAH) in systemic sclerosis (SSc) patients. SSc-derived microparticles also promote vascular inflammation, suggesting a pathogenic role.
Area of Science:
- Cardiovascular Research
- Immunology
- Rheumatology
Background:
- Endothelial microparticles (EMP) are vesicles released from endothelial cells.
- Pulmonary arterial hypertension (PAH) is a serious complication in systemic sclerosis (SSc).
- The role of EMP in SSc-associated PAH and vascular inflammation requires elucidation.
Purpose of the Study:
- To assess the utility of EMP as biomarkers for PAH in SSc patients.
- To investigate the pathogenic role of microparticles (MP) in SSc-related vascular inflammation.
Main Methods:
- Compared EMP levels (CD144+, CD31+, CD62E+, CD143+) in SSc patients with PAH, SSc without PH, and healthy controls.
- Exposed human pulmonary artery endothelial cells (HPAEC) in vitro to MP from SSc patients and controls.
- Measured cytokine and adhesion molecule levels post-MP exposure.
Main Results:
- CD144+ EMP were significantly elevated in SSc-PAH patients (80% diagnostic accuracy).
- SSc patients showed higher CD31+/CD62E+ ratios, indicating increased apoptosis-driven EMP release.
- MP from SSc patients induced increased endothelial inflammation; MP from controls reduced it.
Conclusions:
- CD144+ EMP are potential biomarkers for PAH in SSc.
- Microparticles from SSc patients contribute to endothelial inflammation and may play a pathogenic role in SSc.
More Related Videos
Related Concept Videos
Pulmonary Hypertension: Classification and Pathogenesis
There are various classifications for PH, each relating to different underlying causes and also...
Overview of Systemic and Pulmonary Circulation
The oxygenated blood is sent...
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue,...

