Endothelial Progenitor Cells as a Potential Biomarker in Interstitial Lung Disease Associated with Rheumatoid Arthritis

Interstitial lung disease (ILD) increases morbidity and mortality in patients with rheumatoid arthritis (RA). Although the pathogenesis of ILD associated with RA (RA-ILD+) remains poorly defined, vascular tissue is crucial in lung physiology. In this context, endothelial progenitor cells (EPC) are i...

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Detalles Bibliográficos
Autores: Verónica Pulito-Cueto, Sara Remuzgo-Martínez, Fernanda Genre, Mora Cuesta, Víctor Manuel|||0000-0002-8161-0462, Iturbe Fernández, David|||0000-0002-5241-266X, Sonia Fernández-Rozas, Belén Atienza-Mateo, Leticia Lera-Gómez, Pilar Alonso-Lecue, Javier Rodríguez-Carrio, Diana Prieto-Peña, Virginia Portilla, Blanco Alonso, Ricardo|||0000-0003-2344-2285, Alfonso Corrales, Oreste Gualillo, Cifrián Martínez, José Manuel, López Mejías, Raquel, González-Gay Mantecón, Miguel Ángel
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universidad de Cantabria (UC)
Repositorio:UCrea Repositorio Abierto de la Universidad de Cantabria
Idioma:inglés
OAI Identifier:oai:repositorio.unican.es:10902/21165
Acceso en línea:http://hdl.handle.net/10902/21165
Access Level:acceso abierto
Palabra clave:Endothelial progenitor cells
Vascular damage biomarker
Interstitial lung disease
Rheumatoid arthritis
Idiopathic pulmonary fibrosis
Descripción
Sumario:Interstitial lung disease (ILD) increases morbidity and mortality in patients with rheumatoid arthritis (RA). Although the pathogenesis of ILD associated with RA (RA-ILD+) remains poorly defined, vascular tissue is crucial in lung physiology. In this context, endothelial progenitor cells (EPC) are involved in endothelial tissue repair. However, little is known about their implication in RA-ILD+. Accordingly, we aimed to investigate the potential role of EPC related to endothelial damage in RA-ILD+. EPC quantification in peripheral blood from 80 individuals (20 RA-ILD+ patients, 25 RA-ILD? patients, 21 idiopathic pulmonary fibrosis (IPF) patients, and 14 healthy controls) was performed by flow cytometry. EPC were considered as CD34+, CD45low, CD309+ and CD133+. A significant increase in EPC frequency in RA-ILD+ patients, as well as in RA-ILD? and IPF patients, was found when compared with controls (p < 0.001, p = 0.02 and p < 0.001, respectively). RA-ILD+ patients exhibited a higher EPC frequency than the RA-ILD? ones (p = 0.003), but lower than IPF patients (p < 0.001). Our results suggest that EPC increase may represent a reparative compensatory mechanism in patients with RA-ILD+. The degree of EPC frequency may help to identify the presence of ILD in RA patients and to discriminate RA-ILD+ from IPF

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