Prostaglandin E1 restores endothelial progenitor cell function in systemic sclerosis.

Abstract

Objectives: Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular injury and impaired angiogenesis, with endothelial progenitor cells (EPCs) playing a key role in vascular repair. EPC subsets, including endothelial colony-forming cells (ECFCs) and colony-forming unit-endothelial cells (CFU-ECs), are known to be dysfunctional in SSc, contributing to disease-associated vasculopathy. Prostaglandin E1 (PGE1) is a vasodilator with potential pro-angiogenic effects, but its impact on EPC numbers and function in SSc remains unexplored. This study aimed to investigate whether PGE1 treatment can modulate EPC numbers, specifically CFU-ECs and ECFCs, in patients with SSc and Raynaud's phenomenon (RP), and evaluate its potential role in promoting vascular repair. Methods: This study evaluated the effect of PGE1 on EPC levels in 12 SSc patients with Raynaud's phenomenon (RP) and 5 healthy controls (HCs). CFU-EC and ECFC clusters were quantified before and after PGE1 treatment using standardized culture methods. PGE1 was administered intravenously over 8-9 days. Statistical analyses compared EPC counts between groups and time points.

Results: Baseline CFU-EC and ECFC cluster counts were significantly reduced in SSc patients compared to HCs (p = 0.02 and p < 0.01, respectively). Following PGE1 treatment, both CFU-EC and ECFC clusters significantly increased in SSc patients (p = 0.02 and p = 0.001, respectively), reaching levels comparable to HCs. No significant changes were observed in HCs across two time points. A significant delta in cluster counts was observed in SSc patients versus HCs (CFU-EC: p = 0.03; ECFC: p = 0.01).

Conclusion: PGE1 treatment restores CFU-EC and ECFC levels in SSc patients, suggesting a potential role in repairing vascular damage. These findings highlight PGE1's therapeutic benefits beyond vasodilation, supporting its use in SSc-associated microvasculopathy.