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52. Impact of the Gut Microbiota on Atorvastatin Mediated Effects on Blood Lipids

Author

Zimmermann, Friederike, primary, Roessler, Johann, additional, Schmidt, David, additional, Jasina, Andrzej, additional, Schumann, Paul, additional, Gast, Martina, additional, Poller, Wolfgang, additional, Leistner, David, additional, Giral, Hector, additional, Kränkel, Nicolle, additional, Kratzer, Adelheid, additional, Schuchardt, Sven, additional, Heimesaat, Markus M., additional, Landmesser, Ulf, additional, and Haghikia, Arash, additional

Published
2020
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53. Extracellular vesicle species differentially affect endothelial cell functions and differentially respond to exercise training in patients with chronic coronary syndromes

Author

Kränkel, Nicolle, primary, Strässler, Elisabeth, additional, Uhlemann, Madlen, additional, Müller, Maja, additional, Briand-Schumacher, Sylvie, additional, Klingenberg, Roland, additional, Schulze, P Christian, additional, Adams, Volker, additional, Schuler, Gerhard, additional, Lüscher, Thomas F, additional, Möbius-Winkler, Sven, additional, and Landmesser, Ulf, additional

Published
2020
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54. Structure-function relationships of HDL in diabetes and coronary heart disease

Author

Cardner, Mathias, primary, Yalcinkaya, Mustafa, additional, Goetze, Sandra, additional, Luca, Edlira, additional, Balaz, Miroslav, additional, Hunjadi, Monika, additional, Hartung, Johannes, additional, Shemet, Andrej, additional, Kränkel, Nicolle, additional, Radosavljevic, Silvija, additional, Keel, Michaela, additional, Othman, Alaa, additional, Karsai, Gergely, additional, Hornemann, Thorsten, additional, Claassen, Manfred, additional, Liebisch, Gerhard, additional, Carreira, Erick, additional, Ritsch, Andreas, additional, Landmesser, Ulf, additional, Krützfeldt, Jan, additional, Wolfrum, Christian, additional, Wollscheid, Bernd, additional, Beerenwinkel, Niko, additional, Rohrer, Lucia, additional, and von Eckardstein, Arnold, additional

Published
2020
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56. Propionate attenuates atherosclerosis by immune-dependent regulation of intestinal cholesterol metabolism.

Author

Haghikia, Arash, Zimmermann, Friederike, Schumann, Paul, Jasina, Andrzej, Roessler, Johann, Schmidt, David, Heinze, Philipp, Kaisler, Johannes, Nageswaran, Vanasa, Aigner, Annette, Ceglarek, Uta, Cineus, Roodline, Hegazy, Ahmed N, Vorst, Emiel P C van der, Döring, Yvonne, Strauch, Christopher M, Nemet, Ina, Tremaroli, Valentina, Dwibedi, Chinmay, and Kränkel, Nicolle

Subjects
ATHEROSCLEROSIS, CHOLESTEROL metabolism, PROPIONIC acid, GUT microbiome, GENE expression
Abstract

Aims Atherosclerotic cardiovascular disease (ACVD) is a major cause of mortality and morbidity worldwide, and increased low-density lipoproteins (LDLs) play a critical role in development and progression of atherosclerosis. Here, we examined for the first time gut immunomodulatory effects of the microbiota-derived metabolite propionic acid (PA) on intestinal cholesterol metabolism. Methods and results Using both human and animal model studies, we demonstrate that treatment with PA reduces blood total and LDL cholesterol levels. In apolipoprotein E−/− (Apoe −/−) mice fed a high-fat diet (HFD), PA reduced intestinal cholesterol absorption and aortic atherosclerotic lesion area. Further, PA increased regulatory T-cell numbers and interleukin (IL)-10 levels in the intestinal microenvironment, which in turn suppressed the expression of Niemann-Pick C1-like 1 (Npc1l1), a major intestinal cholesterol transporter. Blockade of IL-10 receptor signalling attenuated the PA-related reduction in total and LDL cholesterol and augmented atherosclerotic lesion severity in the HFD-fed Apoe −/− mice. To translate these preclinical findings to humans, we conducted a randomized, double-blinded, placebo-controlled human study (clinical trial no. NCT03590496). Oral supplementation with 500 mg of PA twice daily over the course of 8 weeks significantly reduced LDL [−15.9 mg/dL (−8.1%) vs. −1.6 mg/dL (−0.5%), P = 0.016], total [−19.6 mg/dL (−7.3%) vs. −5.3 mg/dL (−1.7%), P = 0.014] and non-high-density lipoprotein cholesterol levels [PA vs. placebo: −18.9 mg/dL (−9.1%) vs. −0.6 mg/dL (−0.5%), P = 0.002] in subjects with elevated baseline LDL cholesterol levels. Conclusion Our findings reveal a novel immune-mediated pathway linking the gut microbiota-derived metabolite PA with intestinal Npc1l1 expression and cholesterol homeostasis. The results highlight the gut immune system as a potential therapeutic target to control dyslipidaemia that may introduce a new avenue for prevention of ACVDs. [ABSTRACT FROM AUTHOR]

Published
2022
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57. Personalized exercise prescription in the prevention and treatment of arterial hypertension: a Consensus Document from the European Association of Preventive Cardiology (EAPC) and the ESC Council on Hypertension.

Author

Hanssen, Henner, Boardman, Henry, Deiseroth, Arne, Moholdt, Trine, Simonenko, Maria, Kränkel, Nicolle, Niebauer, Josef, Tiberi, Monica, Abreu, Ana, Solberg, Erik Ekker, Pescatello, Linda, Brguljan, Jana, Coca, Antonio, and Leeson, Paul

Published
2022
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58. Exercise training to reduce cardiovascular risk in patients with metabolic syndrome and type 2 diabetes mellitus: How does it work?

Author

Kränkel, Nicolle, Bahls, Martin, Van Craenenbroeck, Emeline M., Adams, Volker, Serratosa, Luis, Ekker Solberg, Erik, Hansen, Dominique, Dörr, Marcus, Kemps, Hareld, Kränkel, Nicolle, Bahls, Martin, Van Craenenbroeck, Emeline M., Adams, Volker, Serratosa, Luis, Ekker Solberg, Erik, Hansen, Dominique, Dörr, Marcus, and Kemps, Hareld

Abstract

Metabolic syndrome (MetS) – a clustering of pathological conditions, including abdominal obesity, hypertension, dyslipidemia and hyperglycaemia – is closely associated with the development of type 2 diabetes mellitus (T2DM) and a high risk of cardiovascular disease. A combination of multigenetic predisposition and lifestyle choices accounts for the varying inter-individual risk to develop MetS and T2DM, as well as for the individual amount of the increase in cardiovascular risk in those patients. A physically active lifestyle can offset about half of the genetically mediated cardiovascular risk. Yet, the extent to which standardized exercise programmes can reduce cardiovascular risk differs between patients. Exercise parameters, such as frequency, intensity, type and duration or number of repetitions, differentially target metabolic function, vascular healthand physical fitness. In addition, exercise-induced molecular mechanisms are modulated by other patient-specific variables, such as age, diet and medication. This review discusses the molecular and cellular mechanisms underlying the effects of exercise training on cardiovascular risk specifically in patients with MetS and T2DM.

Published
2019

60. Altered interactions between the endothelium and myeloid cells affect the vascular response to injury in patients with cardiovascular disease

Author

Kränkel, Nicolle

Subjects
endothelium, cardiovascular disease, myeloid cells, response to injury, 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit, kinins, SDF-1
Abstract

With the change of life style around the world – increased calorie uptake, less active lifestyle, increased uptake of substances and particles which increase oxidative and inflammatory stress for the endothelium –even greater efforts need to be put into prevention and treatment measures for cardiovascular diseases - the main non-communicable cause of death world-wide. This requires concerted efforts on a scientific as well as population-based pre-clinical and clinical scale. The function of endothelial cells is crucial for both, physiologic as well as pathologic processes and underlies the initiation and progression of cardiovascular diseases. Endothelial cell function in turn is affected and modulated by a variety of cells with paracrine activity, both resident within the vascular wall as well as recruited to a site of vascular injury or to an ischaemic tissue from the circulation. Those „accessory“ cells possess great functional and antigenic flexibility and may therefore be crucial in the pathogenesis of the disease, as well as a valuable tool in understanding disease mechanisms and in therapy. It has been the focus of my work to better understand alterations in the function of cells with paracrine influence on endothelial cell function in patients with cardiovascular disease and in their recruitment to the vascular wall after a local injury. Together with my co-workers, I have developed and optimized ex vivo assays to enable and improve the phenotypic and functional characterization of circulating cell populations obtained from patients as well as healthy controls. Next, I have studied the recruitment of circulating cells to sites of tissue ischaemia as well as vascular injury on a molecular and cellular level. Here, we specifically investigated the role of kinin signalling and SDF-1/CXCR4 signalling as mechanisms to recruit specific subtypes of circulating cells, as well as the alteration of these recruitment processes in the context of acute vascular injury as well as atherosclerosis. In both cases, pharmacologic treatment is available to prevent the degradation of the messenger peptides/proteins by angiotensin-converting enzyme and dipeptidyl peptidase 4. Our findings support the notion that modulating the function of myeloid cells and their selective recruitment can manipulate endothelial ability to mount capillarization and vascular repair processes, and that the altered paracrine profile of those „accessory“ or „regulatory“ cell types greatly contributes to the reduction of endothelial function in patients with cardiovascular diseases. Our ongoing studies elucidate the molecular principles underlying microvesicle-mediated crosstalk between leukocytes and the endothelium, specifically the adherence of microvesicles derived from individual types of leukocytes to endothelial areas of laminar versus disrupted flow. Alterations in microvesicle release by distinct types of leukocytes during therapy might help to monitor therapy adherence and success. Together, these investigations might help optimize target specific delivery of therapeutics, thus enhancing therapy efficiency and limiting side effects., Kardiovaskuläre Erkrankungen stellen aktuell die größte Gruppe nichtübertragbarer Erkrankungen weltweit. Einhergehend mit der weltweiten Änderung des Lebensstils – erhöhte Kalorienaufnahme, verringerte körperliche Aktivität, erhöhte Belastung der Umwelt mit Substanzen und Partikeln, die inflammatorische Reaktionen auslösen und somit chronisch einen Stress auf das Endothel ausüben – werden immer größere Anstrengungen notwendig sein, um die Prävention und Behandlung kardiovaskulärer Erkrankungen zu stärken. Dies erfordert die Zusammenarbeit von Wissenschaftlern und Klinikern auf grundlagenwissenschaftlicher, prä-klinischer und klinischer Ebene, sowie einen engen Bezug zu den Patientenpopulationen. Einschränkungen in der Funktion der Endothelzellen sind grundlegend mit der Initiation und dem Fortschreiten kardiovaskulärer Erkrankungen verbunden. Die Endothelfunktion selbst wird durch verschiedene gewebsständige und zirkulierende Zellen mit parakriner Funktion beeinflusst, was entweder funktionsunterstützend und erhaltend wirken, oder im Gegensatz dazu den Verlust der Endothelfunktion noch beschleunigen kann. Myeloide Zellen mit parakriner Funktion werden bei Gefäßverletzungen oder bei Ischämie aus dem umliegenden Gewebe und aus der Zirkulation rekrutiert und besitzen eine große funktionelle und immunphänotypische Flexibilität. Die vorliegende Arbeit beschäftigt sich mit Veränderungen der Interaktion zwischen parakrin wirkenden, myeloiden Zellen und den Gefäßendothel bei Patienten mit kardiovaskulären Erkrankungen und mit der Rekrutierung bestimmter Leukozytensubtypen an und in die geschädigte Gefäßwand. Es wurden ex vivo-Assays entwickelt und optimiert, welche die phänotypische und funktionelle Charakterisierung zirkulierender Zellpopulationen aus Patienten und gesunden Kontrollprobanden ermöglichen. Zudem wurde die Rekrutierung verscheidener Typen zirkulierender Zellen in ischämisches Gewebe und an die verletzte Gefäßwand untersucht, sowie deren molekulare Mediatoren charakterisiert. Ein Fokus der Arbeiten lag hierbei auf dem Kinin-System und dem SDF-1/CXCR4 Signalweg. In beiden Fällen sind Pharmaka verfügbar, die die Degradation der Mediatoren durch Angiotensin-converting Enzyme und Dipeptidylpeptidase 4 hemmen können. Die Daten unterstützen das Konzept, dass die Modulation der Funktion und der selektiven Rekrutierung myeloider Zellen die Fähigkeit des Endothels unterstützt, die Kappilarisierung und vaskuläre Reparaturprozesse zu initiieren. Weiterhin unterstreichen die Daten die große Bedeutung myeloider Zellen für die Aufrechterhaltung der Funktion der Blutgefäße. Einschränkungen der Kinin- und SDF-1-vermittelten Funktionen bei myeloiden Zellen von Patienten sind daher eng mit Funktionseinschränkungen des Endothels bei Patienten mit kardiovaskulären Erkrankungen verbunden. Weiterführende Studien untersuchen die molekularen Mechanismen der mikrovesikel-basierten Kommunikation zweischen Zelltypen, besonders zwischen myeloiden Zellen und dem Gefäßendothel. Diese Untersuchungen sollen zum Einen die Genauigkeit der verfügbaren diagnostischen Methoden bei der Einschätzung der Progression kardiovaskulärer Erkrankungen und des Erfolges von Therapiemaßnahmen verbessern, zum Anderen zur Entwicklung von Methoden zur zielgerichteten Verabreichung von Pharmaka dienen.

Published
2018

61. Towards a personalised approach in exercise-based cardiovascular rehabilitation: How can translational research help? A ‘call to action’ from the Section on Secondary Prevention and Cardiac Rehabilitation of the European Association of Preventive Cardiology

Author

Gevaert, Andreas B, primary, Adams, Volker, additional, Bahls, Martin, additional, Bowen, T Scott, additional, Cornelissen, Veronique, additional, Dörr, Marcus, additional, Hansen, Dominique, additional, Kemps, Hareld MC, additional, Leeson, Paul, additional, Van Craenenbroeck, Emeline M, additional, and Kränkel, Nicolle, additional

Published
2019
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64. Exercise training for patients with type 2 diabetes and cardiovascular disease: What to pursue and how to do it. A Position Paper of the European Association of Preventive Cardiology (EAPC)

Author

Kemps, Hareld, primary, Kränkel, Nicolle, additional, Dörr, Marcus, additional, Moholdt, Trine, additional, Wilhelm, Matthias, additional, Paneni, Francesco, additional, Serratosa, Luis, additional, Ekker Solberg, Erik, additional, Hansen, Dominique, additional, Halle, Martin, additional, and Guazzi, Marco, additional

Published
2019
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67. Towards a personalised approach in exercise-based cardiovascular rehabilitation: How can translational research help? A 'call to action' from the Section on Secondary Prevention and Cardiac Rehabilitation of the European Association of Preventive Cardiology

Author

Gevaert, Andreas B, Adams, Volker, Bahls, Martin, Bowen, T Scott, Cornelissen, Veronique, Dörr, Marcus, Hansen, Dominique, Kemps, Hareld MC, Leeson, Paul, Van Craenenbroeck, Emeline M, and Kränkel, Nicolle

Published
2020
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75. Vascular repair strategies in type 2 diabetes: novel insights

Author

Kuschnerus, Kira, Landmesser, Ulf, and Kränkel, Nicolle

Subjects
Mini-Review
Abstract

Impaired functions of vascular cells are responsible for the majority of complications in patients with type 2 diabetes (T2D). Recently a better understanding of mechanisms contributing to development of vascular dysfunction and the role of systemic inflammatory activation and functional alterations of several secretory organs, of which adipose tissue has more recently been investigated, has been achieved. Notably, the progression of vascular disease within the context of T2D appears to be driven by a multitude of incremental signaling shifts. Hence, successful therapies need to target several mechanisms in parallel, and over a long time period. This review will summarize the latest molecular strategies and translational developments of cardiovascular therapy in patients with T2D.

Published
2015

77. Increased Expression of miR-483-3p Impairs the Vascular Response to Injury in Type 2 Diabetes.

Author

Kuschnerus, Kira, Straessler, Elisabeth T., Müller, Maja F., Lüscher, Thomas F., Landmesser, Ulf, and Kränkel, Nicolle

Subjects
TYPE 2 diabetes, ZINC-finger proteins, WOUNDS & injuries, TRANSCRIPTION factors
Abstract

Aggravated endothelial injury and impaired endothelial repair capacity contribute to the high cardiovascular risk in patients with type 2 diabetes (T2D), but the underlying mechanisms are still incompletely understood. Here we describe the functional role of a mature form of miRNA (miR) 483-3p, which limits endothelial repair capacity in patients with T2D. Expression of human (hsa)-miR-483-3p was higher in endothelial-supportive M2-type macrophages (M2MΦs) and in the aortic wall of patients with T2D than in control subjects without diabetes. Likewise, the murine (mmu)-miR-483* was higher in T2D than in nondiabetic murine carotid samples. Overexpression of miR-483-3p increased endothelial and macrophage apoptosis and impaired reendothelialization in vitro. The inhibition of hsa-miR-483-3p in human T2D M2MΦs transplanted to athymic nude mice (NMRI-Foxn1ν/Foxn1ν ) or systemic inhibition of mmu-miR-483* in B6.BKS(D)-Leprdb /J diabetic mice rescued diabetes-associated impairment of reendothelialization in the murine carotid-injury model. We identified the endothelial transcription factor vascular endothelial zinc finger 1 (VEZF1) as a direct target of miR-483-3p. VEZF1 expression was reduced in aortae of diabetic mice and upregulated in diabetic murine aortae upon systemic inhibition of mmu-483*. The miRNA miR-483-3p is a critical regulator of endothelial integrity in patients with T2D and may represent a therapeutic target to rescue endothelial regeneration after injury in patients with T2D. [ABSTRACT FROM AUTHOR]

Published
2019
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78. Extracellular vesicle species differentially affect endothelial cell functions and differentially respond to exercise training in patients with chronic coronary syndromes

Author

Kränkel, Nicolle, Strässler, Elisabeth, Uhlemann, Madlen, Müller, Maja, Briand-Schumacher, Sylvie, Klingenberg, Roland, Schulze, P Christian, Adams, Volker, Schuler, Gerhard, Lüscher, Thomas F, Möbius-Winkler, Sven, and Landmesser, Ulf

Abstract

Background Extracellular vesicles are released upon cellular activation and mediate inter-cellular communication. Individual species of extracellular vesicles might have divergent roles in vascular homeostasis and may show different responses to therapies such as exercise training.Aims We examine endothelial effects of medium-size and small extracellular vesicles from the same individual with or without chronic coronary syndrome, and in chronic coronary syndrome patients participating in a four-week high-intensity interval training intervention.Methods Human aortic endothelial cells were exposed to medium-size extracellular vesicles and small extracellular vesicles isolated from plasma samples of study participants. Endothelial cell survival, activation and re-endothelialisation capacity were assessed by respective staining protocols. Extracellular vesicles were quantified by nanoparticle tracking analysis and flow cytometry. Extracellular vesicle microRNA expression was quantified by realtime-quantitative polymerase chain reaction.Results In patients with chronic coronary syndrome (n= 25), plasma counts of leukocyte-derived medium-size extracellular vesicles were higher than in age-matched healthy controls (n= 25; p= 0.04) and were reduced by high-intensity interval training (n= 15; p= 0.01 vs baseline). Re-endothelialisation capacity was promoted by medium-size extracellular vesicles from controls, but not by medium-size extracellular vesicles from chronic coronary syndrome patients. High-intensity interval training for 4 weeks enhanced medium-size extracellular vesicle-mediated support of in vitro re-endothelialisation. Small extracellular vesicles from controls or chronic coronary syndrome patients increased endothelial cell death and reduced repair functions and were not affected by high-intensity interval training.Conclusion The present study demonstrates that medium-size extracellular vesicles and small extracellular vesicles differentially affect endothelial cell survival and repair responses. This equilibrium is unbalanced in patients with chronic coronary syndrome where leukocyte-derived medium-size extracellular vesicles are increased leading to a loss of medium-size extracellular vesicle-mediated endothelial repair. High-intensity interval training partially restored medium-size extracellular vesicle-mediated endothelial repair, underlining its use in cardiovascular prevention and therapy to improve endothelial function.

Published
2024
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79. Exercise training in women with cardiovascular disease: Differential response and barriers – review and perspective

Author

Witvrouwen, Isabel, Van Craenenbroeck, Emeline M, Abreu, Ana, Moholdt, Trine, and Kränkel, Nicolle

Abstract

Background Exercise-based cardiac rehabilitation has a class 1A recommendation in coronary artery disease and heart failure based on its beneficial effects on mortality, morbidity and quality of life. However, the inter-individual response to exercise training is highly variable and influenced by both training and patient characteristics. Notably, men and women display a different training response, even when accounting for age, height and lean muscle mass. Most studies investigating exercise effects on various physiological outcomes focus on male patients. Because women are understudied, the scientific evidence for tailored exercise prescription in women is still limited.Methods This narrative review summarises: (a) the underlying physiological determinants of the response to exercise training in women with cardiovascular disease, in which women rely more on fat than on carbohydrate oxidation during exercise, have lower aerobic capacities and smaller increases in cardiac function during exercise; (b) the benefits and barriers of exercise in women, in whom improving cardiometabolic risk and quality of life is weighed against socioeconomic and psychological needs; and (c) the relevance of different clinical endpoints in exercise trials such as maximum oxygen uptake, morbidity, mortality, training characteristics, quality of life and metabolic or vascular endpoints.Results Finally, we provide a perspective on how to improve referral, enrolment and adherence to exercise training in women, with structured approaches to inform the referring physician as well as the patient, and offering more flexible, gender-tailored or tele/smartphone-based programmes while addressing the socioeconomic and psychological needs of the patients. This may ultimately improve the admission, adherence and outcome of exercise-based cardiac rehabilitation in women.

Published
2024
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83. Migration towards SDF-1 selects angiogenin-expressing bone marrow monocytes endowed with cardiac reparative activity in patients with previous myocardial infarction

Author

Ascione, Raimondo, primary, Rowlinson, Jonathan, additional, Avolio, Elisa, additional, Katare, Rajesh, additional, Meloni, Marco, additional, Spencer, Helen L, additional, Mangialardi, Giuseppe, additional, Norris, Caroline, additional, Kränkel, Nicolle, additional, Spinetti, Gaia, additional, Emanueli, Costanza, additional, and Madeddu, Paolo, additional

Published
2015
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85. Short-term inhibition of DPP-4 enhances endothelial regeneration after acute arterial injury via enhanced recruitment of circulating progenitor cells

Author

Brenner, Christoph, primary, Kränkel, Nicolle, additional, Kühlenthal, Sarah, additional, Israel, Lars, additional, Remm, Friederike, additional, Fischer, Cornelia, additional, Herbach, Nadja, additional, Speer, Timo, additional, Grabmaier, Ulrich, additional, Laskowski, Alexandra, additional, Gross, Lisa, additional, Theiss, Hans, additional, Wanke, Rüdiger, additional, Landmesser, Ulf, additional, and Franz, Wolfgang-Michael, additional

Published
2014
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86. Novel insights into the critical role of bradykinin and the kinin b2 receptor for vascular recruitment of circulating endothelial repair-promoting mononuclear cell subsets: alterations in patients with coronary disease

Author

Kränkel, Nicolle, Kuschnerus, Kira, Müller, Maja, Speer, Timo, Mocharla, Pavani, Madeddu, Paolo, Bader, Michael, Lüscher, Thomas F, Landmesser, Ulf, Kränkel, Nicolle, Kuschnerus, Kira, Müller, Maja, Speer, Timo, Mocharla, Pavani, Madeddu, Paolo, Bader, Michael, Lüscher, Thomas F, and Landmesser, Ulf

Abstract

BACKGROUND: Endothelial injury is considered critical for progression of atherosclerosis and its complications in coronary artery disease (CAD). The endothelial-supportive effects of bradykinin have mainly been attributed to activation of the resident endothelium. Here we newly investigate the role of bradykinin and its B2 receptor for the recruitment and functional activation of circulating mononuclear cell subsets with endothelial-repair promoting capacity, such as CD34(+)CXCR4(+)cells, at sites of arterial injury. METHODS AND RESULTS: Bradykinin-B2-receptor (B2R) blockade by icatibant substantially impaired recruitment of circulating CD34(+)CXCR4(+) mononuclear cells (expressing high levels of B2R) to endothelial cells in vitro and to injured arterial wall in vivo, whereas recruitment of CD14(hi) monocytes (expressing low levels of B2R) was unchanged. Moreover, the capacity of genetically B2R-deficient bone marrow cells to promote endothelial repair in vivo was markedly impaired as compared with wild-type bone marrow cells. B2R expression was reduced on CD34(+)CXCR4(+)mononuclear cells and endothelial repair-promoting early outgrowth cells, but not on CD14(hi)monocytes, from CAD patients as compared with healthy subjects. B2R stimulation induced CD18 activation in early outgrowth cells of healthy subjects, but not in early outgrowth cells of CAD patients. Adenoviral B2R overexpression enhanced in vivo vascular recruitment and rescued impaired endothelial repair capacity of early outgrowth cells from CAD patients. CONCLUSIONS: We newly report that bradykinin/B2R signaling may promote endothelial repair after arterial injury by selective recruitment and functional activation of B2R-expressing circulating mononuclear cell subsets. In CAD patients, B2R downregulation on endothelial repair-promoting circulating mononuclear cells substantially impairs the bradykinin-dependent endothelial repair, representing a novel mechanism promoting endothelial injury in CAD patient

Published
2013

87. Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells from Patients with Chronic Heart Failure: Role for Impaired in vivo Neovascularization and Cardiac Repair Capacity

Author

Jakob, Philipp, Doerries, Carola, Briand, Sylvie, Mocharla, Pavani, Kränkel, Nicolle, Besler, Christian, Mueller, Maja, Manes, Costantina, Templin, Christian, Baltes, Christof, Rudin, Markus, Adams, Heiner, Wolfrum, Mathias, Noll, Georg, Ruschitzka, Frank, Lüscher, Thomas F; https://orcid.org/0000-0002-5259-538X, Landmesser, Ulf, Jakob, Philipp, Doerries, Carola, Briand, Sylvie, Mocharla, Pavani, Kränkel, Nicolle, Besler, Christian, Mueller, Maja, Manes, Costantina, Templin, Christian, Baltes, Christof, Rudin, Markus, Adams, Heiner, Wolfrum, Mathias, Noll, Georg, Ruschitzka, Frank, Lüscher, Thomas F; https://orcid.org/0000-0002-5259-538X, and Landmesser, Ulf

Abstract

BACKGROUND: MicroRNAs are key regulators of angiogenic processes. Administration of angiogenic early outgrowth cells (EOCs) or CD34(+)-cells has been suggested to improve cardiac function after ischemic injury in particular by promoting neovascularization. The present study therefore examines regulation of angiomiRs, microRNAs involved in angiogenesis, in angiogenic-EOCs and circulating CD34(+)-cells from patients with chronic heart failure (CHF) and the role for their cardiac repair capacity. METHODS AND RESULTS: Angiogenic-EOCs and CD34(+)-cells were isolated from patients with CHF due to ischemic cardiomyopathy (n=45) and healthy subjects (HS; n=35). In flow-cytometry analyses angiogenic-EOCs were largely myeloid and positive for alternatively-activated, M2-macrophage markers. In vivo cardiac neovascularization and functional repair capacity were examined after transplantation into nude mice with myocardial infarction (MI). Cardiac transplantation of angiogenic-EOCs from HS markedly increased neovascularization and improved cardiac function, whereas no such effect was observed after transplantation of angiogenic-EOCs from patients with CHF. RT-PCR analysis of 14 candidate angiomiRs, expressed in angiogenic-EOCs, revealed a pronounced loss of angiomiR-126 and -130a in angiogenic-EOCs from patients with CHF, that was also observed in circulating CD34(+)-cells. Anti-miR-126 transfection markedly impaired the capacity of angiogenic-EOCs from HS to improve cardiac function. miR-126-mimic transfection increased the capacity of angiogenic-EOCs from patients with CHF to improve cardiac neovascularization and function. CONCLUSIONS: The present study reveals a loss of angiomiR-126 and -130a in angiogenic-EOCs and circulating CD34(+)-cells from patients with CHF. Reduced miR-126 expression was identified as a novel mechanism limiting their capacity to improve cardiac neovascularization and function that can be targeted by miR-126-mimic-transfection.

Published
2012

90. Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells From Patients With Chronic Heart Failure

Author

Jakob, Philipp, primary, Doerries, Carola, additional, Briand, Sylvie, additional, Mocharla, Pavani, additional, Kränkel, Nicolle, additional, Besler, Christian, additional, Mueller, Maja, additional, Manes, Costantina, additional, Templin, Christian, additional, Baltes, Christof, additional, Rudin, Markus, additional, Adams, Heiner, additional, Wolfrum, Mathias, additional, Noll, Georg, additional, Ruschitzka, Frank, additional, Lüscher, Thomas F., additional, and Landmesser, Ulf, additional

Published
2012
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91. Abstract 18317: Abnormal High Density Lipoprotein (HDL) from Patients with Chronic Kidney Disease (CKD) Increases Arterial Blood Pressure: Role of Toll-Like Receptor-2 (TLR-2)

Author

Speer, Timo, primary, Rohrer, Lucia, additional, Blyszczuk, Przemyslaw, additional, Kränkel, Nicolle, additional, Kuschnerus, Kira, additional, Shi, Yi, additional, Akhmedov, Alexander, additional, Zewinger, Stephen, additional, von Eckardstein, Arnold, additional, Lúscher, Thomas, additional, Bahlmann, Ferdinand, additional, Fliser, Danilo, additional, and Landmesser, Ulf, additional

Published
2012
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92. Deletion of L-Selectin Increases Atherosclerosis Development in ApoE−/− Mice

Author

Rozenberg, Izabela, primary, Sluka, Susanna H. M., additional, Mocharla, Pavani, additional, Hallenberg, Anders, additional, Rotzius, Pierre, additional, Borén, Jan, additional, Kränkel, Nicolle, additional, Landmesser, Ulf, additional, Borsig, Lubor, additional, Lüscher, Thomas F., additional, Eriksson, Einar E., additional, and Tanner, Felix C., additional

Published
2011
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94. Tissue Kallikrein Is Essential for Invasive Capacity of Circulating Proangiogenic Cells

Author

Spinetti, Gaia, primary, Fortunato, Orazio, additional, Cordella, Daniela, additional, Portararo, Paola, additional, Kränkel, Nicolle, additional, Katare, Rajesh, additional, Sala-Newby, Graciela B., additional, Richer, Christine, additional, Vincent, Marie-Pascale, additional, Alhenc-Gelas, Francois, additional, Tonolo, Giancarlo, additional, Cherchi, Sara, additional, Emanueli, Costanza, additional, and Madeddu, Paolo, additional

Published
2011
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95. High-dose rosuvastatin in chronic heart failure promotes vasculogenesis, corrects endothelial function, and improves cardiac remodeling — Results from a randomized, double-blind, and placebo-controlled study

Author

Erbs, Sandra, primary, Beck, Ephraim B., additional, Linke, Axel, additional, Adams, Volker, additional, Gielen, Stephan, additional, Kränkel, Nicolle, additional, Möbius-Winkler, Sven, additional, Höllriegel, Robert, additional, Thiele, Holger, additional, Hambrecht, Rainer, additional, and Schuler, Gerhard, additional

Published
2011
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96. Exercise Training in Patients With Advanced Chronic Heart Failure (NYHA IIIb) Promotes Restoration of Peripheral Vasomotor Function, Induction of Endogenous Regeneration, and Improvement of Left Ventricular Function

Author

Erbs, Sandra, primary, Höllriegel, Robert, additional, Linke, Axel, additional, Beck, Ephraim B., additional, Adams, Volker, additional, Gielen, Stephan, additional, Möbius-Winkler, Sven, additional, Sandri, Marcus, additional, Kränkel, Nicolle, additional, Hambrecht, Rainer, additional, and Schuler, Gerhard, additional

Published
2010
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100. Human CD133 + Progenitor Cells Promote the Healing of Diabetic Ischemic Ulcers by Paracrine Stimulation of Angiogenesis and Activation of Wnt Signaling

Author

Barcelos, Lucíola S., primary, Duplaa, Cécile, additional, Kränkel, Nicolle, additional, Graiani, Gallia, additional, Invernici, Gloria, additional, Katare, Rajesh, additional, Siragusa, Mauro, additional, Meloni, Marco, additional, Campesi, Ilaria, additional, Monica, Manuela, additional, Simm, Andreas, additional, Campagnolo, Paola, additional, Mangialardi, Giuseppe, additional, Stevanato, Lara, additional, Alessandri, Giulio, additional, Emanueli, Costanza, additional, and Madeddu, Paolo, additional

Published
2009
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