Session Type: Poster Session (Sunday)
Session Time: 9:00AM-11:00AM
Background/Purpose: Interstitial lung disease (ILD) is one of the most significant comorbidities that contributes to the increased mortality observed in patients with rheumatoid arthritis (RA) [1,2]. Although the pathogenesis of ILD associated to RA (RA-ILD) remains poorly defined , it is known that vascular tissue plays a crucial role in lung physiology . In this context, a population of cells termed endothelial progenitor cells (EPC) are involved in vasculogenesis and endothelial tissue repair . Previous reports suggest the implication of EPC in different conditions such as RA and idiopathic pulmonary fibrosis (IPF), the most common and destructive ILD [5,6]. Nevertheless, little is known about their specific role in RA-ILD. Accordingly, the purpose of this study was to shed light on the potential role of EPC in RA-ILD pathophysiology.
Methods: Peripheral venous blood was collected from a total of 30 patients (13 with RA-ILD, 5 with RA without ILD and 12 with IPF) as well as 13 healthy controls. All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC by flow cytometry was analyzed for the expression of surface antigens. The combination of antibodies against the stem cell marker CD34, the immature progenitor marker CD133, the endothelial marker VEGF receptor 2 (CD309) and the common leukocyte antigen CD45 was used. EPC were considered as CD34+, CD45Low, CD309+ and CD133+. All statistical analyses were performed using Prism software 5 (GraphPad).
Results: EPC frequency was significantly increased in RA patients, with and without ILD, and IPF patients when compared to controls (p< 0.0001, p= 0.004 and p< 0.0001, respectively). Nevertheless, patients with RA, in particular those with RA-ILD, showed a lower frequency of EPC than those with IPF (p=0.009).
Conclusion: Our results provide evidence for a potential role of EPC in the pathophysiology of RA-ILD disease.
 Current Rheumatology Reports 2003; 5:278-286;  Arthritis & Rheumatology 2015; 67: 28-38;  Nature protocols 2015; 10: 1697-1708;  Science 1997; 275: 964-966;  Rheumatology 2012; 51: 1775-1784;  Angiogenesis 2013; 16: 147-157.
VP-C is supported by funds of a PREVAL18/01 (IDIVAL). SR-M is supported by funds of the RETICS Program (RD16/0012/0009), co-funded by the European Regional Development Fund (ERDF). VM is supported by funds of a Miguel Servet type I programme (grant CP16/00033) (ISCIII, co-funded by ESF). RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, “Investing in your future”) (grant CP16/00033).
To cite this abstract in AMA style:Pulito-Cueto V, Remuzgo-Martínez S, Genre F, Lera-Gomez L, Mijares V, Alonso Lecue P, Mora Cuesta V, Iturbe D, Fernández Rozas S, Blanco R, Corrales A, Cifrian Martínez J, López-Mejías R, Gonzalez-Gay M. Endothelial Progenitor Cells in the Pathophysiology of Interstitial Lung Disease Associated with Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/endothelial-progenitor-cells-in-the-pathophysiology-of-interstitial-lung-disease-associated-with-rheumatoid-arthritis/. Accessed November 26, 2020.
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