AB0094 INCREASE OF ENDOTHELIAL PROGENITOR CELLS IN SYSTEMIC SCLEROSIS-ASSOCIATED INTERSTITIAL LUNG DISEASE
Authors: V. Pulito-Cueto, S. Remuzgo Martinez, F. Genre, B. Atienza-Mateo, V. M. Mora-Cuesta, D. Iturbe-Fernández, L. Lera-Gómez, R. Pérez-Fernández, D. Prieto-Peña, V. Portilla, R. Blanco, A. Corrales, J. M. Cifrián-Martínez, R. López-Mejías, M. A. González-Gay
Journal: Annals of the Rheumatic Diseases (2021)

Background: Endothelial progenitor cells (EPC), involved in vasculogenesis and endothelial tissue repair, have been described as relevant players in vascular and connective tissue diseases [1-2]. In this regard, a previous study of our group disclosed that the degree of EPC frequency may help to identify the presence of interstitial lung disease (ILD) in rheumatoid arthritis patients [3]. Given that ILD is the main cause of mortality in patients with systemic sclerosis (SSc) [1, 4-6], the understanding of the role of EPC in the mechanism of SSc-ILD + vasculopathy is crucial. Objectives: To assess the potential role of EPC on vascular dysfunction associated with the presence of ILD in patients with SSc. Methods: Peripheral venous blood was collected from a total of 39 patients with SSc, 20 with ILD (SSc-ILD + ) and 19 without ILD (SSc-ILD - ). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by flow cytometry. EPC were considered as CD34 + , CD45 Low , CD309 + and CD133 + . Results: Statistically significant differences in EPC frequency between patients with SSc-ILD + and patients with SSc-ILD - were disclosed. Specifically, an increase of EPC frequency was observed in SSc-ILD + patients when compared to patients with SSc-ILD - (mean ± standard deviation: 0.033 ± 0.012 versus 0.021 ± 0.017, respectively, p=0.012). Conclusion: Our results suggest a potential role of EPC on vascular damage associated with the manifestation of ILD in patients with SSc. References: [1]Eur J Rheumatol 2020;7(Suppl 3):S139-S146. [2]Arthritis Rheum 2009;60(11):3168-79. [3]J Clin Med 2020;9(12):4098. [4]Ann Rheum Dis 2007;66(7):940-4. [5]Rheumatology (Oxford) 2010;49(12):2375-80. [6]Eur Respir Rev 2015;24(135):102-14. Acknowledgements: Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF). Disclosure of Interests: Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD