scholarly journals SAT0014 ENDOTHELIAL PROGENITOR CELLS: ROLE IN ENDOTHELIAL DAMAGE OF INTERSTITIAL LUNG DISEASE ASSOCIATED TO RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 937.1-937
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo-Martínez ◽  
F. Genre ◽  
V. M. Mora-Cuesta ◽  
D. Iturbe Fernández ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Endothelial Damage ◽  
Research Support ◽  
Endothelial Progenitor

Background:Interstitial lung disease (ILD) is one of the most significant comorbidities of rheumatoid arthritis (RA), increasing the mortality in these patients [1,2]. Although the pathogenesis of ILD associated to RA (RA-ILD+) remains poorly defined [1], it is known that vascular tissue plays a crucial role in lung physiology [3]. In this context, a population of cells termed endothelial progenitor cells (EPC) are involved in vasculogenesis and endothelial tissue repair [4]. 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+.Objectives:The purpose of this study was to shed light on the potential role of EPC in endothelial damage in RA-ILD+.Methods:Peripheral venous blood was collected from a total of 68 individuals (18 with RA-ILD+, 17 with RA-ILD-, 19 with IPF and 14 healthy controls). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by the expression of surface antigens by flow cytometry. 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 patients with RA-ILD+, RA-ILD-and IPF compared to controls (p=0.001, p=0.002, p< 0.0001, respectively). Nevertheless, patients with RA, both RA-ILD+and RA-ILD-, showed a lower frequency of EPC than those with IPF (p= 0.048, p= 0.006, respectively).Conclusion:Our results provide evidence for a potential role of EPC as a reparative compensatory mechanism related to endothelial damage in RA-ILD+, RA-ILD-and IPF patients. Interestingly, EPC frequency may help to establish a differential diagnostic between patients with IPF and those who have an underlying autoimmune disease (RA-ILD+).References:[1] J Clin Med 2019; 8: 2038;[2] Arthritis Rheumatol 2015; 67: 28-38;[3] Nat Protoc 2015; 10: 1697-1708;[4] Science 1997; 275: 964-966;[5] Rheumatology (Oxford) 2012; 51: 1775-1784;[6] Angiogenesis 2013; 16: 147-157.Acknowledgments:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: PI18/00042 (ISCIII-ERDF); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo-Martínez: None declared, Fernanda Genre: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe Fernández: None declared, Sonia Fernández-Rozas: None declared, Leticia Lera-Gómez: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Belén Atienza-Mateo: None declared, Virginia Portilla: None declared, David Merino: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, Roche, Consultant of: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD, Speakers bureau: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma. MSD, Alfonso Corrales Speakers bureau: Abbvie, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD

scholarly journals AB0094 INCREASE OF ENDOTHELIAL PROGENITOR CELLS IN SYSTEMIC SCLEROSIS-ASSOCIATED INTERSTITIAL LUNG DISEASE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1076.1-1076
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo Martinez ◽  
F. Genre ◽  
B. Atienza-Mateo ◽  
V. M. Mora-Cuesta ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Type I ◽  
Research Support ◽  
Endothelial Progenitor

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+, CD45Low, 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

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

2020 ◽  
Vol 9 (12) ◽  
pp. 4098
Author(s):  
Verónica Pulito-Cueto ◽  
Sara Remuzgo-Martínez ◽  
Fernanda Genre ◽  
Víctor M. Mora-Cuesta ◽  
David Iturbe-Fernández ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Tissue ◽  
Endothelial Damage ◽  
Compensatory Mechanism ◽  
Endothelial Progenitor ◽  
Potential Biomarker

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.

Potential role of endothelial progenitor cells in the pathophysiology of heart failure: Clinical implications and perspectives

2006 ◽  
Vol 189 (2) ◽  
pp. 247-254 ◽  
Author(s):  
Ioannis Andreou ◽  
Dimitris Tousoulis ◽  
Costas Tentolouris ◽  
Charalambos Antoniades ◽  
Christodoulos Stefanadis
Keyword(s):  
Heart Failure ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Clinical Implications ◽  
Endothelial Progenitor

3045Role of osteogenic circulating endothelial progenitor cells in dissemination of large arterial calcification in rheumatoid arthritis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y.-H Chan ◽  
M C Ngai ◽  
Y Chen ◽  
M Z Wu ◽  
Y J Yu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Arterial Calcification ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells ◽  
Calcium Load ◽  
Contrast Ct ◽  
Carotid Calcification

Abstract Background Rheumatoid arthritis is associated with both abnormal bone metabolism and atherogenesis but mechanistic links were missing. Aim This study aimed to investigate the role of osteocalcin (OCN)-expressing circulating endothelial progenitor cells (EPC)s in the severity and dissemination of systemic arterial calcifications in rheumatoid arthritis. Methods We performed flow cytometry studies in 145 consecutive patients with rheumatoid arthritis to determine osteogenic circulating levels of OCN-positive (OCN+) CD34+KDR+ and OCN+CD34+, versus conventional early EPC CD34+CD133+KDR+. Total calcium load of the thoracic aorta (ascending plus descending) and the carotid arteries were assessed by non-contrast computed tomography (CT) and contrast CT angiography. Results Osteogenic EPCs OCN+CD34+KDR+ (P=0.002) and OCN+CD34+ were strikingly associated with the clustered presence of aortic and carotid calcification (P=0.002 and 0.001 respectively, Figure). Multivariable analyses revealed that circulating OCN+CD34+KDR+ (B=14.4 [95% CI 4.0 to 24.8], P=0.007) and OCN+CD34+ (B=9.6 [95% CI 4.9 to 14.3], P<0.001) remained independently associated with increased aortic calcium load. OCN+CD34+ EPC (B=0.8 [95% CI 0.1 to 1.5], P=0.023), but not OCN+CD34+KDR+ EPC (B=1.2 [95% CI −0.2 to 2.6], P=0.09) was further independently associated with carotid calcium load. In comparison, conventional early EPC CD34+CD133+KDR+ had no significant association with aortic or carotid calcium load (P=0.46 and 0.88, respectively). Conclusions Circulating level of osteogenic EPC is associated with promulgated aortic and carotid calcification in patients with rheumatoid arthritis, suggesting a potential mechanistic role of the bone-vascular axis in pro-atherogenicity of rheumatic diseases. Acknowledgement/Funding General Research Fund, Hong Kong Research Grants Council

scholarly journals Endothelial Progenitor Cells and Rheumatoid Arthritis: Response to Endothelial Dysfunction and Clinical Evidences

2021 ◽  
Vol 22 (24) ◽  
pp. 13675
Author(s):  
Klara Komici ◽  
Angelica Perna ◽  
Aldo Rocca ◽  
Leonardo Bencivenga ◽  
Giuseppe Rengo ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Activation ◽  
Endothelial Damage ◽  
Current Evidence ◽  
Endothelial Progenitor ◽  
Cardiovascular Comorbidities ◽  
And Function ◽  
Endothelial Integrity

Rheumatoid Arthritis (RA) is a chronic autoimmune inflammatory disease characterized by the swelling of multiple joints, pain and stiffness, and accelerated atherosclerosis. Sustained immune response and chronic inflammation, which characterize RA, may induce endothelial activation, damage and dysfunction. An equilibrium between endothelial damage and repair, together with the preservation of endothelial integrity, is of crucial importance for the homeostasis of endothelium. Endothelial Progenitor Cells (EPCs) represent a heterogenous cell population, characterized by the ability to differentiate into mature endothelial cells (ECs), which contribute to vascular homeostasis, neovascularization and endothelial repair. A modification of the number and function of EPCs has been described in numerous chronic inflammatory and auto-immune conditions; however, reports that focus on the number and functions of EPCs in RA are characterized by conflicting results, and discrepancies exist among different studies. In the present review, the authors describe EPCs’ role and response to RA-related endothelial modification, with the aim of illustrating current evidence regarding the level of EPCs and their function in this disease, to summarize EPCs’ role as a biomarker in cardiovascular comorbidities related to RA, and finally, to discuss the modulation of EPCs secondary to RA therapy.

scholarly journals Potential Role of Caveolin-1 in Regulating the Function of Endothelial Progenitor Cells from Experimental MODS Model

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Tianhang Luo ◽  
Jixin Shu ◽  
Zhengmao Lu ◽  
Ting Han ◽  
Guoen Fang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Multiple Organ ◽  
Cost Of Care ◽  
Endothelial Progenitor ◽  
Caveolin 1 ◽  
Organ Repair

Multiple organ dysfunction syndrome (MODS) remains a great challenge in critical care because of its common occurrence, high cost of care, and high mortality. Vascular endothelial injury is the initiation step in the development of MODS, and EPCs are essential for the process of organ repair. It is unclear whether and how caveolin-1 (Cav-1) in EPCs contributes to the pathogenesis of MODS. The present study is aimed at investigating the potential role of Cav-1 in EPCs during MODS. We established a MODS model in pigs, isolated and characterized EPCs from the MODS model, and tracked Cav-1 expression and various in vitro behaviors of EPCs from the MODS model. Then, we knockdown Cav-1 expression with siRNA or induce Cav-1 expression with proinflammatory factors to evaluate potential effects on EPCs. Our results suggest that Cav-1 expression correlated with EPC functions during MODS and Cav-1 regulates the function of endothelial progenitor cells via PI3K/Akt/eNOS signaling during MODS. Thus, Cav-1 in EPCs could be an attractive target for the treatment of MODS.

scholarly journals Endothelial progenitor cells: Origin and role of angiogenesis in cardiovascular diseases

2021 ◽  
Vol 36 (2) ◽  
pp. 23-29
Author(s):  
O. A. Denisenko ◽  
S. P. Chumakova ◽  
O. I. Urazova
Keyword(s):  
Cardiovascular Diseases ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Damage ◽  
Cell Populations ◽  
Endothelial Progenitor ◽  
Vascular Integrity ◽  
Treatment Algorithms ◽  
Artery Disease

Endothelial progenitor cells (EPCs) are the cells that play a key role in maintaining vascular integrity and repairing endothelial damage. It has been shown that EPCs can differentiate into mature endothelial cells and are also capable of producing various regulatory growth factors and cytokines. There are many studies focusing on the associations between coronary artery disease and circulating EPCs. However, it is still challenging to use EPCs for the development of diagnostic and treatment algorithms in cardiovascular diseases. This review presents data on EPCs subtypes, methods for obtaining them, biological characteristics of cell populations, and the factors of EPCs mobilization to the site of injury in cardiovascular diseases.

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