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Potential biomarkers in patients with systemic sclerosis
Andrea Delle Sedie1, Lucrezia Riente1, Lavinia Maggiorini2
1Rheumatology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
International Journal of Rheumatic Diseases
|October 13, 2017
Summary
Systemic sclerosis (SSc) involves reduced blood vessel growth. This study found elevated endostatin, elastase, and adhesion molecules (sICAM-1, sVCAM-1) in SSc patients, suggesting their role in disease pathogenesis.
Area of Science:
- Vascular biology
- Immunology
- Rheumatology
Background:
- Systemic sclerosis (SSc) is characterized by reduced capillary density, leading to tissue hypoxia.
- Hypoxia typically triggers angiogenesis, but the mediators involved in SSc remain unclear.
Purpose of the Study:
- To investigate mediators regulating angiogenesis in SSc.
- To correlate mediator levels with serological and clinical parameters in SSc patients.
Main Methods:
- Quantified levels of vascular endothelial growth factor, fibroblast growth factor-2, endostatin, thrombospondin-1, and soluble adhesion molecules (sICAM-1, sVCAM-1) using ELISA.
- Compared mediator levels between SSc patients and healthy controls.
Main Results:
- Endostatin levels were significantly higher in SSc patients compared to controls.
- Elastase, a protease involved in endostatin production, was also increased in SSc.
- Soluble adhesion molecules sICAM-1 and sVCAM-1 were elevated in SSc and correlated with each other.
- sICAM-1 positively correlated with inflammatory markers C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).
Conclusions:
- Endostatin, elastase, sICAM-1, and sVCAM-1 are implicated in the pathogenesis of SSc.
- sICAM-1 may serve as a biomarker for the inflammatory status in SSc due to its correlation with CRP and ESR.