Prostaglandin E1 restores endothelial progenitor cell function in systemic sclerosis.

Abstract

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 RP, and evaluate its potential role in promoting vascular repair. This study evaluated the effect of PGE1 on EPC levels in 12 SSc patients with RP and five 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 the groups and time points. Baseline CFU-EC and ECFC cluster counts were significantly reduced in SSc patients compared with 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 vs. HCs (CFU-EC: P = 0.03; ECFC: P = 0.01). 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.