P750Role of circulating endothelial cells post-heart transplantation

Abstract Background The role of endothelial progenitor cells (EPC) in heart transplantation (HT) is not well defined. Thus, the aim of this study was to evaluate prospectively the dynamic changes of circulating EPC levels in relation to post-HT rejection risk. Methods There were 27 HT recipients who had EPC from peripheral blood quantified during 6 months follow-up after HT. Patients were monitored regularly, by right ventricular endomyocardial biopsy assessment, for cellular rejection (ACR) defined as grade ≥2 or an antibody-mediated rejection (AMR) characterized by histopathological changes recorded as AMR1H. The primary end-point was acute rejection, either AMR or ACR. Results ACR and AMR were observed in 7 (25.9%) and 6 (22.2%) subjects respectively. EPC levels, after logarithmic transformation, immediately post-HT were alike regardless of ACR status, however patients with lower EPC were at risk of AMR at 1 month (Table 1). On the other hand patients with a significant reduction of EPC at 1 month post-HT compared with HT were less likely to have either ACR or AMR (p=0.0003). During longer post-HT observation (12 months) patients had similar EPC levels regardless of the rejection events. Dynamic changes in EPC levels are presented in figure. Nonetheless, greater changes in EPC expressed by coefficient of variation were associated with the risk of either AMR or ACR compared to the participants without rejection (mean [lower–upper quartile]) 15 [13–18] vs 8 [5–13]; p=0.02) and (22 [14–26] vs 8 [5–13]; p=0.01) respectively. EPC by rejection – 1st month following HT ACR (+) AMR (+) ACR (−) and AMR (−) p^ p p N=3 (mean± SD) N=4 (mean± SD) N=20 (mean± SD) ACR (+) vs ACR (−) and AMR (−) AMR (+) vs ACR (−) and AMR (−) EPC log HT 5.14±1.55 3.81±1.01 5.30±0.88 0.0325 0.97 0.025 EPC log M1 4.97±0.59 3.69±1.33 4.15±1.29 0.4160 0.55 0.78 Delta EPC log M1-HT -0.17±1.98* −0.12±1.30* −1.15±1.18# 0.2195 0.44 0.32 ACR – acute cellular rejection; AMR or – acute antibody-mediated rejection; EPC log – endothelial progenitor cells after logarithmic transformation; HT – within 24 hours post-transplantation; M1 – at 1-month post-transplantation; Delta EPC log M1-HT – difference in EPC log between M1 and HT. #p=0.0003 for the difference between M1 vs HT; *p=ns for the difference between M1 vs HT; ^pP – for the difference among the groups. Changes in EPC level post-HT Conclusions Early reduction of EPC levels was predictive of a lower risk of ACR or AMR. Greater dynamic changes of EPC during 6 months of observation were associated with a higher risk of rejection suggesting an important role of EPC in the pathological processes post-HT. Thus our findings suggest significant role of EPC post-HT with respect to rejection status. Acknowledgement/Funding Intramural research grant from the Institute of Cardiology

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The Functional Role of Macrophage Migration Inhibitory Factor in the Recruitment of Endothelial Progenitor Cells in Patients during Cardiac Surgery

The Thoracic and Cardiovascular Surgeon ◽

10.1055/s-0035-1544513 ◽

2015 ◽

Vol 63 (S 01) ◽

Author(s):

L. Hammer ◽

S. Kraemer ◽

C. Emontzpohl ◽

J. Bernhagen ◽

A. Goetzenich ◽

...

Keyword(s):

Cardiac Surgery ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Migration Inhibitory Factor ◽

Functional Role ◽

Macrophage Migration Inhibitory Factor ◽

Inhibitory Factor ◽

Macrophage Migration ◽

Endothelial Progenitor

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Cigarette Smoking and Angiogenesis: What is the Role of Endothelial Progenitor Cells?

Current Angiogenesis ◽

10.2174/2211552811201030236 ◽

2012 ◽

Vol 1 (3) ◽

pp. 236-242 ◽

Cited By ~ 1

Author(s):

Emilio Centaro ◽

Linda Landini ◽

Aurelio Leone

Keyword(s):

Cigarette Smoking ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Progenitor

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

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2020-eular.3228 ◽

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

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Effective Actions of Ion Release from Mesoporous Bioactive Glass and Macrophage Mediators on the Differentiation of Osteoprogenitor and Endothelial Progenitor Cells

Pharmaceutics ◽

10.3390/pharmaceutics13081152 ◽

2021 ◽

Vol 13 (8) ◽

pp. 1152

Author(s):

Alberto Polo-Montalvo ◽

Laura Casarrubios ◽

María Concepción Serrano ◽

Adrián Sanvicente ◽

María José Feito ◽

...

Keyword(s):

Bone Regeneration ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Mesoporous Structure ◽

Ion Release ◽

Endothelial Progenitor ◽

Matrix Mineralization ◽

Intracellular Content

Due to their specific mesoporous structure and large surface area, mesoporous bioactive glasses (MBGs) possess both drug-delivery ability and effective ionic release to promote bone regeneration by stimulating osteogenesis and angiogenesis. Macrophages secrete mediators that can affect both processes, depending on their phenotype. In this work, the action of ion release from MBG-75S, with a molar composition of 75SiO2-20CaO-5P2O5, on osteogenesis and angiogenesis and the modulatory role of macrophages have been assessed in vitro with MC3T3-E1 pre-osteoblasts and endothelial progenitor cells (EPCs) in monoculture and in coculture with RAW 264.7 macrophages. Ca2+, phosphorous, and silicon ions released from MBG-75S were measured in the culture medium during both differentiation processes. Alkaline phosphatase activity and matrix mineralization were quantified as the key markers of osteogenic differentiation in MC3T3-E1 cells. The expression of CD31, CD34, VEGFR2, eNOS, and vWF was evaluated to characterize the EPC differentiation into mature endothelial cells. Other cellular parameters analyzed included the cell size and complexity, intracellular calcium, and intracellular content of the reactive oxygen species. The results obtained indicate that the ions released by MBG-75S promote osteogenesis and angiogenesis in vitro, evidencing a macrophage inhibitory role in these processes and demonstrating the high potential of MBG-75S for the preparation of implants for bone regeneration.

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