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  1. Book ; Online ; Thesis: Identifizierung neuer Schubspannungs-regulierter Gene mittels "Atlas cDNA Expression Array"

    Urbich, Carmen

    Bedeutung für die Funktion von Endothelzellen

    2001  

    Author's details von Carmen Urbich
    Language German
    Size Online-Ressource
    Edition [Elektronische Ressource]
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Univ., Diss--Frankfurt (Main), 2001
    Database Former special subject collection: coastal and deep sea fishing

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  2. Book ; Online ; Thesis: Identifizierung neuer Schubspannungs-regulierter Gene mittels "Atlas cDNA Expression Array"

    Urbich, Carmen [Verfasser]

    Bedeutung für die Funktion von Endothelzellen

    2001  

    Author's details von Carmen Urbich
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article: Risk factors for coronary artery disease, circulating endothelial progenitor cells, and the role of HMG-CoA reductase inhibitors.

    Urbich, Carmen / Dimmeler, Stefanie

    Kidney international

    2005  Volume 67, Issue 5, Page(s) 1672–1676

    Abstract: Recent studies suggest that postnatal neovascularization relies not exclusively on sprouting of preexisting vessels ("angiogenesis"), but also involves the contribution of bone marrow-derived circulating endothelial progenitor cells (EPCs). EPCs can be ... ...

    Abstract Recent studies suggest that postnatal neovascularization relies not exclusively on sprouting of preexisting vessels ("angiogenesis"), but also involves the contribution of bone marrow-derived circulating endothelial progenitor cells (EPCs). EPCs can be isolated from peripheral blood or bone marrow mononuclear cells, CD34(+) or CD133(+) hematopoietic progenitors. Infusion of EPCs was shown to promote postnatal neovascularization of ischemic tissue after myocardial infarction in animal models and initial clinical trials. Moreover, circulating endothelial precursor cells can home to denuded arteries after balloon injury and contribute to endothelial regeneration, thereby limiting the development of restenosis. Thus, circulating endothelial cells may exert an important function as endogenous repair mechanism to maintain the integrity of the endothelial monolayer and to promote ischemia-induced neovascularization. However, risk factors for coronary artery disease, such as diabetes, hypercholesterolemia, and hypertension are associated with impaired number and function of EPC in patients with coronary artery disease. Therapeutically, the reduction of EPC number and the decreased functional activity in patients with coronary artery disease was counteracted by 3-hydroxy-3-methylglutaryl coenzymeA (HMG-CoA) reductase inhibitors (statins), vascular endothelial growth factor (VEGF), estrogen, or exercise. At the molecular level, these factors are well established to activate the phosphatidyl-inositol-3-kinase (PI3K)-Akt-dependent activation of the endothelial nitric oxide synthase (eNOS), suggesting that the PI3K-Akt-eNOS signaling pathway may be involved in the transduction of atheroprotective factors. Taken together, the balance of atheroprotective and proatherosclerotic factors may influence EPC levels and their functional capacity to improve neovascularization and endothelial regeneration.
    MeSH term(s) Animals ; Coronary Artery Disease/drug therapy ; Coronary Artery Disease/etiology ; Coronary Artery Disease/pathology ; Endothelium, Vascular/pathology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Mice ; Models, Cardiovascular ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Risk Factors ; Signal Transduction ; Stem Cells/pathology ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Vascular Endothelial Growth Factor A ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39)
    Language English
    Publishing date 2005-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1111/j.1523-1755.2005.00261.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: CD40 and vascular inflammation.

    Urbich, Carmen / Dimmeler, Stefanie

    The Canadian journal of cardiology

    2004  Volume 20, Issue 7, Page(s) 681–683

    Abstract: Atherosclerosis is currently considered a chronic inflammatory disease combined with a disorder of lipid metabolism and deposition. Risk factors for coronary disease, as well as circulating cytokines, are involved in endothelial activation, leading to an ...

    Abstract Atherosclerosis is currently considered a chronic inflammatory disease combined with a disorder of lipid metabolism and deposition. Risk factors for coronary disease, as well as circulating cytokines, are involved in endothelial activation, leading to an adhesive and dysfunctional endothelium. The CD40 receptor (CD40) and its counterpart, the CD40 ligand (CD40L/CD154), were originally found to regulate T cell-dependent B cell differentiation. Meanwhile, several studies clearly demonstrate that the CD40/CD40L system plays an important role not only in cellular immunity and inflammation, but also in the pathophysiology of atherosclerosis. This is evidenced by the finding that inhibition of CD40/CD40L interaction prevents atherogenesis in animal models. Thus, the regulation of proatherogenic factors including CD40L may provide novel therapeutic options to treat inflammatory disorders such as atherosclerosis.
    MeSH term(s) Animals ; CD40 Antigens/metabolism ; CD40 Antigens/physiology ; CD40 Ligand/metabolism ; CD40 Ligand/physiology ; Coronary Artery Disease/immunology ; Coronary Artery Disease/metabolism ; Coronary Artery Disease/physiopathology ; Cytokines/metabolism ; Disease Progression ; Endothelium, Vascular/immunology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Humans ; Vasculitis/immunology ; Vasculitis/metabolism ; Vasculitis/physiopathology
    Chemical Substances CD40 Antigens ; Cytokines ; CD40 Ligand (147205-72-9)
    Language English
    Publishing date 2004-05-15
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Endothelial progenitor cells functional characterization.

    Urbich, Carmen / Dimmeler, Stefanie

    Trends in cardiovascular medicine

    2004  Volume 14, Issue 8, Page(s) 318–322

    Abstract: Increasing evidence suggests that circulating progenitor cells contribute to postnatal neovascularization. These cells home to sites of ischemia, adopt an endothelial phenotype, and contribute to new blood vessel formation. Hence, the identity of the ... ...

    Abstract Increasing evidence suggests that circulating progenitor cells contribute to postnatal neovascularization. These cells home to sites of ischemia, adopt an endothelial phenotype, and contribute to new blood vessel formation. Hence, the identity of the circulating cells that contribute to neovascularization is not entirely clear. Bone-marrow-derived hematopoietic progenitor cells can give rise to endothelial cells and contribute to endothelial recovery and new capillary formation after ischemia. However, nonhematopoietic stem cells within the bone marrow and adipose-tissue-derived cells, as well as cardiac and neural progenitor cells, also differentiate to endothelial cells. Progenitor cells from the different sources may be useful to augment therapeutic vascularization. The present review article summarizes the different subtypes of (endothelial) progenitor cells that can give rise to endothelial cells, enhance neovascularization, and may be suitable for therapeutic neovascularization.
    MeSH term(s) Animals ; Bone Marrow/embryology ; Bone Marrow Cells/cytology ; Cell Lineage ; Endothelium, Vascular/embryology ; Fetal Blood/cytology ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/physiology ; Mesenchymal Stromal Cells/physiology ; Neovascularization, Physiologic
    Language English
    Publishing date 2004-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1097434-9
    ISSN 1873-2615 ; 1050-1738
    ISSN (online) 1873-2615
    ISSN 1050-1738
    DOI 10.1016/j.tcm.2004.10.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Endothelial progenitor cells: characterization and role in vascular biology.

    Urbich, Carmen / Dimmeler, Stefanie

    Circulation research

    2004  Volume 95, Issue 4, Page(s) 343–353

    Abstract: Infusion of different hematopoietic stem cell populations and ex vivo expanded endothelial progenitor cells augments neovascularization of tissue after ischemia and contributes to reendothelialization after endothelial injury, thereby, providing a novel ... ...

    Abstract Infusion of different hematopoietic stem cell populations and ex vivo expanded endothelial progenitor cells augments neovascularization of tissue after ischemia and contributes to reendothelialization after endothelial injury, thereby, providing a novel therapeutic option. However, controversy exists with respect to the identification and the origin of endothelial progenitor cells. Overall, there is consensus that endothelial progenitor cells can derive from the bone marrow and that CD133/VEGFR2 cells represent a population with endothelial progenitor capacity. However, increasing evidence suggests that there are additional bone marrow-derived cell populations (eg, myeloid cells, "side population" cells, and mesenchymal cells) and non-bone marrow-derived cells, which also can give rise to endothelial cells. The characterization of the different progenitor cell populations and their functional properties are discussed. Mobilization and endothelial progenitor cell-mediated neovascularization is critically regulated. Stimulatory (eg, statins and exercise) or inhibitory factors (risk factors for coronary artery disease) modulate progenitor cell levels and, thereby, affect the vascular repair capacity. Moreover, recruitment and incorporation of endothelial progenitor cells requires a coordinated sequence of multistep adhesive and signaling events including adhesion and migration (eg, by integrins), chemoattraction (eg, by SDF-1/CXCR4), and finally the differentiation to endothelial cells. This review summarizes the mechanisms regulating endothelial progenitor cell-mediated neovascularization and reendothelialization.
    MeSH term(s) Animals ; Antigens, CD/analysis ; Bone Marrow Cells/cytology ; Cell Adhesion ; Cell Differentiation ; Cell Lineage ; Cell Movement ; Cells, Cultured/cytology ; Endothelial Cells/cytology ; Endothelium, Vascular/cytology ; Growth Substances/pharmacology ; Growth Substances/physiology ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/classification ; Hematopoietic Stem Cells/physiology ; Hindlimb/blood supply ; Humans ; Ischemia/physiopathology ; Ischemia/therapy ; Mesenchymal Stromal Cells/physiology ; Myeloid Progenitor Cells/cytology ; Neovascularization, Physiologic ; Pluripotent Stem Cells/cytology ; Rats
    Chemical Substances Antigens, CD ; Growth Substances
    Language English
    Publishing date 2004-08-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/01.RES.0000137877.89448.78
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Homing and engraftment of progenitor cells: a prerequisite for cell therapy.

    Chavakis, Emmanouil / Urbich, Carmen / Dimmeler, Stefanie

    Journal of molecular and cellular cardiology

    2008  Volume 45, Issue 4, Page(s) 514–522

    Abstract: Cell therapy is a promising therapeutic option for treating patients with ischemic diseases. The efficiency of cell therapy to augment recovery after ischemia depends on the sufficient recruitment of applied cells to the target tissue. Using in vivo ... ...

    Abstract Cell therapy is a promising therapeutic option for treating patients with ischemic diseases. The efficiency of cell therapy to augment recovery after ischemia depends on the sufficient recruitment of applied cells to the target tissue. Using in vivo imaging techniques the extent of homing was shown to be rather low in most experimental and clinical studies. The elucidation of the molecular mechanisms of homing of different progenitor cell subpopulation to sites of injury is essential for the development of new specific therapeutic strategies, in order to improve the efficacy of cell-based therapies. Homing to sites of active neovascularization is a complex process depending on a timely and spatially orchestrated interplay between chemokines (e.g. SDF-1), chemokine receptors, intracellular signaling, adhesion molecules (selectins and integrins) and proteases. The review will focus on the mechanisms underlying homing of adult bone marrow-derived hematopoietic cells, mesenchymal stem cells, and vasculogenic circulating cells and discuss strategies how to optimize cell engraftment.
    MeSH term(s) Animals ; Cell Adhesion Molecules/metabolism ; Cell Movement ; Cell Transplantation ; Chemokines/metabolism ; Graft Survival ; Hematopoietic Stem Cells/metabolism ; Humans ; Mesenchymal Stromal Cells/metabolism ; Myocardial Ischemia/metabolism ; Myocardial Ischemia/therapy ; Neovascularization, Physiologic ; Receptors, Chemokine/metabolism
    Chemical Substances Cell Adhesion Molecules ; Chemokines ; Receptors, Chemokine
    Language English
    Publishing date 2008-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2008.01.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Targeting microRNA expression to regulate angiogenesis.

    Kuehbacher, Angelika / Urbich, Carmen / Dimmeler, Stefanie

    Trends in pharmacological sciences

    2008  Volume 29, Issue 1, Page(s) 12–15

    Abstract: MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression at the post-transcriptional level by either degradation or translational repression of a target mRNA. More than 400 miRNAs have been identified in the human genome, but the ... ...

    Abstract MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression at the post-transcriptional level by either degradation or translational repression of a target mRNA. More than 400 miRNAs have been identified in the human genome, but the relevance of most of them to physiological and pathological processes remains unclear. Although downregulation of the miRNA-processing enzymes Dicer and Drosha is known to impair angiogenesis, only a few specific miRNAs targeting endothelial cell function and angiogenesis have been identified. miR-221 and miR-222 block endothelial cell migration, proliferation and angiogenesis in vitro by targeting the stem cell factor receptor c-Kit and indirectly regulating expression of endothelial nitric oxide synthase. A pro-angiogenic function has been established for the miR-17-92 cluster, which promotes tumor angiogenesis in vivo. Expression of let7-f and miR-27b contributes to in vitro angiogenesis. We review recent studies on the involvement of miRNA in angiogenesis and discuss their implications for miRNA-based therapeutic strategies targeting this process in disease.
    MeSH term(s) Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/physiopathology ; Drug Delivery Systems ; Gene Expression Regulation/drug effects ; Humans ; MicroRNAs/drug effects ; MicroRNAs/metabolism ; Neoplasms/drug therapy ; Neoplasms/physiopathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/physiopathology ; Neovascularization, Physiologic/physiology
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2008-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2007.10.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Role of microRNAs in vascular diseases, inflammation, and angiogenesis.

    Urbich, Carmen / Kuehbacher, Angelika / Dimmeler, Stefanie

    Cardiovascular research

    2008  Volume 79, Issue 4, Page(s) 581–588

    Abstract: The integrity of the endothelial monolayer is fundamental for the homoeostasis of the vascular system. Functional endothelial cells are also required for the growth of new blood vessels during neovascularization. Although multiple growth factors have ... ...

    Abstract The integrity of the endothelial monolayer is fundamental for the homoeostasis of the vascular system. Functional endothelial cells are also required for the growth of new blood vessels during neovascularization. Although multiple growth factors have been shown to regulate angiogenesis and vascular development, little is known about the complex upstream regulation of gene expression and translation. MicroRNAs (miRNAs) are an emerging class of highly conserved, non-coding small RNAs that regulate gene expression on the post-transcriptional level by inhibiting the translation of protein from mRNA or by promoting the degradation of mRNA. More than 500 human miRNAs have been identified so far, and increasing evidence indicates that miRNAs have distinct expression profiles and play crucial roles in various physiological and pathological processes such as cardiogenesis, haematopoietic lineage differentiation, and oncogenesis. Meanwhile, a few specific miRNAs that regulate endothelial cell functions and angiogenesis have been described. Let7-f, miR-27b, and mir-130a were identified as pro-angiogenic miRNAs. In contrast, miR-221 and miR-222 inhibit endothelial cell migration, proliferation, and angiogenesis in vitro by targeting the stem cell factor receptor c-kit and indirectly regulating endothelial nitric oxide synthase expression. Moreover, some miRNAs are involved in tumour angiogenesis such as the miR-17-92 cluster and miR-378. Early studies also indicate the contribution of specific miRNAs (e.g. miR-155, miR-21, and miR-126) to vascular inflammation and diseases. Thus, the identification of miRNAs and their respective targets may offer new therapeutic strategies to treat vascular diseases such as atherosclerosis, to improve neovascularization after ischaemia, or to prevent tumour progression.
    MeSH term(s) Animals ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/metabolism ; Gene Expression Regulation ; Genetic Therapy ; Humans ; Inflammation/genetics ; Inflammation/physiopathology ; Inflammation/therapy ; MicroRNAs/metabolism ; Neovascularization, Physiologic/genetics ; RNA Processing, Post-Transcriptional ; Ribonuclease III/metabolism ; Vascular Diseases/genetics ; Vascular Diseases/physiopathology ; Vascular Diseases/therapy
    Chemical Substances MicroRNAs ; DROSHA protein, human (EC 3.1.26.3) ; Drosha protein, mouse (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3)
    Language English
    Publishing date 2008-09-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvn156
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Restoration of cardiac function with progenitor cells.

    Urbich, Carmen / Rössig, Lothar / Dimmeler, Stefanie

    Novartis Foundation symposium

    2006  Volume 274, Page(s) 214–23; discussion 223–7, 272–6

    Abstract: The biological limitations to cardiac regenerative growth create a clinical need to promote more efficient cardiac repair. Experimental studies and early-phase clinical trials indicate that progenitor cells may be useful as a therapeutic tool to improve ... ...

    Abstract The biological limitations to cardiac regenerative growth create a clinical need to promote more efficient cardiac repair. Experimental studies and early-phase clinical trials indicate that progenitor cells may be useful as a therapeutic tool to improve heart function after myocardial ischaemia. This paper will summarize experimental studies to determine (1) the mechanisms underlying progenitor cell homing to ischaemic tissue and (2) to define transcription factors involved in endothelial maturation of progenitor cells. Homing seems to be assisted by a proteolytic enzyme, cathepsin L, which degrades the extracellular matrix. In an in vitro assay, a cathepsin inhibitor prevented different progenitor cell populations from passing through a matrigel layer. In vivo, progenitor cells lacking cathepsin L had an impaired capacity to promote neovascularization in ischaemic mouse limbs compared with normal, wild-type cells. Differentiation of progenitor cells towards the endothelial phenotype involves a member of the homeobox gene family, HoxA9. HoxA9 regulates endothelial gene expression (eNOS, KDR, VE-cadherin). Moreover, HoxA9-deficient mice have a severe impairment of neovascularization capacity after ischaemia. In the second part of the paper, we describe clinical studies using bone marrow or the peripheral blood-derived cells for functional recovery of patients with acute and chronic heart failure (TOPCARE-AMI, TOPCARE-CHF). Whereas blood-derived and bone marrow-derived progenitor cells were equally effective in patients with acute myocardial infarction, bone marrow-derived cells were significantly better than blood-derived progenitor cells in patients with chronic ischaemic heart disease.
    MeSH term(s) Animals ; Bone Marrow Cells/metabolism ; Cell Differentiation ; Cell Lineage ; Clinical Trials as Topic ; Humans ; Ischemia/pathology ; Mice ; Models, Biological ; Myocardial Infarction/pathology ; Myocardial Infarction/therapy ; Myocardial Ischemia/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Stem Cell Transplantation ; Stem Cells/cytology ; Stem Cells/metabolism ; Transcription Factors/metabolism
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2006
    Publishing country England
    Document type Journal Article ; Review
    ISSN 1528-2511
    ISSN 1528-2511
    Database MEDical Literature Analysis and Retrieval System OnLINE

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