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

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 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.

A cardiac rehabilitation program increases the acute respond of endothelial progenitor cells after maximum exercise in patients with chronic heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Kourek ◽  
E Karatzanos ◽  
D Delis ◽  
M Alshamari ◽  
V Linardatou ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Cardiac Rehabilitation ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Rehabilitation Program ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Maximum Exercise

Abstract Background Chronic heart failure (CHF) remains a leading cause of morbidity and mortality and it is characterized by vascular endothelial dysfunction. During the last decades, endothelial progenitor cells (EPCs) are being used as an index of the endothelium restoration potential, therefore reflecting the vascular endothelial function. Exercise training has been shown to stimulate the mobilization of EPCs at rest in CHF patients. However, the effect of exercise training on the acute respond of EPCs after maximum exercise in CHF patients remains unknown. Purpose The purpose of the study was to assess the effect of a cardiac rehabilitation (CR) program on the acute respond of EPCs after maximum exercise in patients with CHF. Methods Forty-four consecutive patients (35 males) with stable CHF [mean±SD, Age (years): 56±10, BMI (kg/m2): 28.7±5.2, EF (%): 33±8, Peak VO2 (ml/kg/min): 18.4±4.4, Peak work rate (watts): 101±39] enrolled a 36-session CR program based on high-intensity interval exercise training. All patients underwent an initial symptom limited maximal cardiopulmonary exercise testing (CPET) on an ergometer before the CR program and a final maximal CPET after the CR program. Venous blood was drawn before and after each CPET. Five circulating endothelial populations were identified and quantified by flow cytometry; CD34+/CD45-/CD133+, CD34+/CD45-/CD133+/VEGFR2, CD34+/CD133+/VEGFR2, CD34+/CD45-/CD133- and CD34+/CD45-/CD133-/VEGFR2. EPCs values are expressed as cells/million enucleated cells in medians (25th-75th percentiles). Results The acute mobilization of EPCs after the final CPET was higher than after the initial CPET in 4 out of 5 circulating endothelial populations. Most specifically, difference of the acute mobilization of CD34+/CD45-/CD133+ cells [initial CPET: 25 (15–46) vs final CPET: 49 (26–71), p=0.002], CD34+/CD45-/CD133+/VEGFR2 cells [initial CPET: 3 (2–5) vs final CPET: 8 (5–12), p&lt;0.001], CD34+/CD45-/CD133- cells [initial CPET: 129 (52–338) vs final CPET: 250 (129–518), p=0.03] and CD34+/CD45-/CD133-/VEGFR2 cells [initial CPET: 2 (1–4) vs final CPET: 6 (3–9), p&lt;0.001] increased after the final CPET. The acute mobilization of CD34+/CD133+/VEGFR2 cells [initial CPET: 3 (−1–7) vs final CPET: 5 (0–15), p=0.441] did not differ between the 2 CPETS. Conclusion A 36-session cardiac rehabilitation program increases the acute respond of endothelial progenitor cells after maximum cardiopulmonary exercise training in patients with chronic heart failure, therefore indicating the beneficial effect of exercise training on the vascular endothelial function. Funding Acknowledgement Type of funding source: Public grant(s) – EU funding. Main funding source(s): Co-financed by Greece and the European Union (European Social Fund- ESF) through the Operational Programme “Human Resources Development, Education and Lifelong Learning” in the context of the project

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