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  1. Article ; Online: Interdependence of Angiogenesis and Arteriogenesis in Development and Disease.

    le Noble, Ferdinand / Kupatt, Christian

    International journal of molecular sciences

    2022  Volume 23, Issue 7

    Abstract: The structure of arterial networks is optimized to allow efficient flow delivery to metabolically active tissues. Optimization of flow delivery is a continuous process involving synchronization of the structure and function of the microcirculation with ... ...

    Abstract The structure of arterial networks is optimized to allow efficient flow delivery to metabolically active tissues. Optimization of flow delivery is a continuous process involving synchronization of the structure and function of the microcirculation with the upstream arterial network. Risk factors for ischemic cardiovascular diseases, such as diabetes mellitus and hyperlipidemia, adversely affect endothelial function, induce capillary regression, and disrupt the micro- to macrocirculation cross-talk. We provide evidence showing that this loss of synchronization reduces arterial collateral network recruitment upon arterial stenosis, and the long-term clinical outcome of current revascularization strategies in these patient cohorts. We describe mechanisms and signals contributing to synchronized growth of micro- and macrocirculation in development and upon ischemic challenges in the adult organism and identify potential therapeutic targets. We conclude that a long-term successful revascularization strategy should aim at both removing obstructions in the proximal part of the arterial tree and restoring "bottom-up" vascular communication.
    MeSH term(s) Adult ; Arteries ; Collateral Circulation ; Humans ; Ischemia ; Neovascularization, Pathologic ; Neovascularization, Physiologic
    Language English
    Publishing date 2022-03-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23073879
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Thymosin ß4 and MRTF-A mitigate vessel regression despite cardiovascular risk factors.

    Kupatt, Christian / Ziegler, Tilman / Bähr, Andrea / Le Noble, Ferdinand

    International immunopharmacology

    2023  Volume 117, Page(s) 109786

    Abstract: Since clinical revascularization techniques of coronary or peripheral artery disease (CAD/PAD) focus on macrovessels of the heart, the microcirculatory compartment largely goes unnoticed. However, cardiovascular risk factors not only drive large vessel ... ...

    Abstract Since clinical revascularization techniques of coronary or peripheral artery disease (CAD/PAD) focus on macrovessels of the heart, the microcirculatory compartment largely goes unnoticed. However, cardiovascular risk factors not only drive large vessel atherosclerosis, but also microcirculatory rarefaction, an instance unmet by current therapeutic schemes. Angiogenic gene therapy has the potential to reverse capillary rarefaction, but only if the disease-causing inflammation and vessel-destabilization are addressed. This review summarizes the current knowledge with regard to capillary rarefaction due to cardiovascular risk factors. Moreover, the potential of Thymosin ß4 (Tß4) and its downstream signal, myocardin-related transcription factor-A (MRTF-A), to counteract capillary rarefaction are discussed.
    MeSH term(s) Humans ; Cardiovascular Diseases/drug therapy ; Thymosin/therapeutic use ; Microvascular Rarefaction ; Microcirculation ; Risk Factors ; Coronary Artery Disease ; Heart Disease Risk Factors
    Chemical Substances myocardin ; Thymosin (61512-21-8)
    Language English
    Publishing date 2023-02-20
    Publishing country Netherlands
    Document type Review ; Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2023.109786
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  3. Article ; Online: VEGF (Vascular Endothelial Growth Factor) Inhibition and Hypertension: Does Microvascular Rarefaction Play a Role?

    le Noble, Ferdinand A C / Mourad, Jean-Jacques / Levy, Bernard I / Struijker-Boudier, Harry A J

    Hypertension (Dallas, Tex. : 1979)

    2023  Volume 80, Issue 5, Page(s) 901–911

    Abstract: Drugs acting by inhibition of the angiogenic action of VEGF (vascular endothelial growth factor) have become major instruments in the treatment of cancer. The downside of their favorable effects in cancer treatment is their frequent cardiovascular side ... ...

    Abstract Drugs acting by inhibition of the angiogenic action of VEGF (vascular endothelial growth factor) have become major instruments in the treatment of cancer. The downside of their favorable effects in cancer treatment is their frequent cardiovascular side effects. The most consistent finding thus far on the cardiovascular side effects of VEGF inhibitors is the high incidence of hypertension. In this short review, we discuss the evidence that hypertension occurring during VEGF inhibitor treatment is caused by microvascular rarefaction. After a review of the role of VEGF in microvascular growth and differentiation, we present evidence from studies in experimental models of hypertension as well as clinical studies on the microvascular network changes during and after VEGF inhibitor treatment.
    MeSH term(s) Humans ; Vascular Endothelial Growth Factor A/metabolism ; Microvascular Rarefaction/chemically induced ; Microvascular Rarefaction/complications ; Microvascular Rarefaction/drug therapy ; Hypertension ; Vascular Endothelial Growth Factors ; Neoplasms/drug therapy ; Angiogenesis Inhibitors/adverse effects
    Chemical Substances Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Angiogenesis Inhibitors
    Language English
    Publishing date 2023-02-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.122.19427
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    Zs.A 1488: Show issues Location:
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  4. Article: A defined clathrin-mediated trafficking pathway regulates sFLT1/VEGFR1 secretion from endothelial cells.

    Kinghorn, Karina / Gill, Amy / Marvin, Allison / Li, Renee / Quigley, Kaitlyn / le Noble, Ferdinand / Mac Gabhann, Feilim / Bautch, Victoria L

    bioRxiv : the preprint server for biology

    2023  

    Abstract: FLT1/VEGFR1 negatively regulates VEGF-A signaling and is required for proper vessel morphogenesis during vascular development and vessel homeostasis. Although a soluble isoform, sFLT1, is often mis-regulated in disease and aging, how sFLT1 is trafficked ... ...

    Abstract FLT1/VEGFR1 negatively regulates VEGF-A signaling and is required for proper vessel morphogenesis during vascular development and vessel homeostasis. Although a soluble isoform, sFLT1, is often mis-regulated in disease and aging, how sFLT1 is trafficked and secreted from endothelial cells is not well understood. Here we define requirements for constitutive sFLT1 trafficking and secretion in endothelial cells from the Golgi to the plasma membrane, and we show that sFLT1 secretion requires clathrin at or near the Golgi. Perturbations that affect sFLT1 trafficking blunted endothelial cell secretion and promoted intracellular mis-localization in cells and zebrafish embryos. siRNA-mediated depletion of specific trafficking components revealed requirements for RAB27A, VAMP3, and STX3 for post-Golgi vesicle trafficking and sFLT1 secretion, while STX6, ARF1, and AP1 were required at the Golgi. Depletion of STX6 altered vessel sprouting in a 3D angiogenesis model, indicating that endothelial cell sFLT1 secretion is important for proper vessel sprouting. Thus, specific trafficking components provide a secretory path from the Golgi to the plasma membrane for sFLT1 in endothelial cells that utilizes a specialized clathrin-dependent intermediate, suggesting novel therapeutic targets.
    Language English
    Publishing date 2023-01-28
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.27.525517
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book ; Online: Collateral growth: role of Thymosin B4 and Notch

    Le Noble, Ferdinand

    Standortprojekt/Säule A/Säule B/Säule C: Säule B ; Laufzeit des Projektes: 01.01.2013 - 30.06.2014

    2013  

    Author's details Autor Bericht/Projektleiter: Ferdinand le Noble
    Language German
    Size Online-Ressource (5 S., 151,29 KB)
    Publisher Technische Informationsbibliothek u. Universitätsbibliothek ; Max Delbrueck Center for Molecular Medicine (MDC)
    Publishing place Hannover ; Berlin
    Document type Book ; Online
    Note Förderkennzeichen BMU 81X2100104 ; Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  6. Article ; Online: Parenchymal cues define Vegfa-driven venous angiogenesis by activating a sprouting competent venous endothelial subtype.

    Préau, Laetitia / Lischke, Anna / Merkel, Melanie / Oegel, Neslihan / Weissenbruch, Maria / Michael, Andria / Park, Hongryeol / Gradl, Dietmar / Kupatt, Christian / le Noble, Ferdinand

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 3118

    Abstract: Formation of organo-typical vascular networks requires cross-talk between differentiating parenchymal cells and developing blood vessels. Here we identify a Vegfa driven venous sprouting process involving parenchymal to vein cross-talk regulating venous ... ...

    Abstract Formation of organo-typical vascular networks requires cross-talk between differentiating parenchymal cells and developing blood vessels. Here we identify a Vegfa driven venous sprouting process involving parenchymal to vein cross-talk regulating venous endothelial Vegfa signaling strength and subsequent formation of a specialized angiogenic cell, prefabricated with an intact lumen and pericyte coverage, termed L-Tip cell. L-Tip cell selection in the venous domain requires genetic interaction between vascular Aplnra and Kdrl in a subset of venous endothelial cells and exposure to parenchymal derived Vegfa and Apelin. Parenchymal Esm1 controls the spatial positioning of venous sprouting by fine-tuning local Vegfa availability. These findings may provide a conceptual framework for understanding how Vegfa generates organo-typical vascular networks based on the selection of competent endothelial cells, induced via spatio-temporal control of endothelial Kdrl signaling strength involving multiple parenchymal derived cues generated in a tissue dependent metabolic context.
    MeSH term(s) Angiogenesis ; Endothelial Cells/metabolism ; Neovascularization, Physiologic/genetics ; Veins
    Language English
    Publishing date 2024-04-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-47434-x
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  7. Article: Micro-RNA 92a as a Therapeutic Target for Cardiac Microvascular Dysfunction in Diabetes.

    Samak, Mostafa / Kaltenborn, Diana / Kues, Andreas / Le Noble, Ferdinand / Hinkel, Rabea / Germena, Giulia

    Biomedicines

    2021  Volume 10, Issue 1

    Abstract: Microvascular dysfunction is a pathological hallmark of diabetes, and is central to the ethology of diabetes-associated cardiac events. Herein, previous studies have highlighted the role of the vasoactive micro-RNA 92a (miR-92a) in small, as well as ... ...

    Abstract Microvascular dysfunction is a pathological hallmark of diabetes, and is central to the ethology of diabetes-associated cardiac events. Herein, previous studies have highlighted the role of the vasoactive micro-RNA 92a (miR-92a) in small, as well as large, animal models. In this study, we explore the effects of miR-92a on mouse and human cardiac microvascular endothelial cells (MCMEC, HCMEC), and its underlying molecular mechanisms. Diabetic HCMEC displayed impaired angiogenesis and a pronounced inflammatory phenotype. Quantitative PCR (qPCR) showed an upregulation of miR-92a in primary diabetic HCMEC. Downregulation of miR-92a by antagomir transfection in diabetic HCMEC rescued angiogenesis and ameliorated diabetic endothelial bed inflammation. Furthermore, additional analysis of potential in silico-identified miR-92a targets in diabetic HCMEC revealed the miR-92a dependent downregulation of an essential metalloprotease, ADAM10. Accordingly, downregulation of ADAM10 impaired angiogenesis and wound healing in MCMEC. In myocardial tissue slices from diabetic pigs, ADAM10 dysregulation in micro- and macro-vasculature could be shown. Altogether, our data demonstrate the role of miR-92a in cardiac microvascular dysfunction and inflammation in diabetes. Moreover, we describe for the first time the metalloprotease ADAM10 as a novel miR-92a target, mediating its anti-angiogenic effect.
    Language English
    Publishing date 2021-12-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10010058
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  8. Article ; Online: A defined clathrin-mediated trafficking pathway regulates sFLT1/VEGFR1 secretion from endothelial cells.

    Kinghorn, Karina / Gill, Amy / Marvin, Allison / Li, Renee / Quigley, Kaitlyn / Singh, Simcha / Gore, Michaelanthony T / le Noble, Ferdinand / Gabhann, Feilim Mac / Bautch, Victoria L

    Angiogenesis

    2023  Volume 27, Issue 1, Page(s) 67–89

    Abstract: FLT1/VEGFR1 negatively regulates VEGF-A signaling and is required for proper vessel morphogenesis during vascular development and vessel homeostasis. Although a soluble isoform, sFLT1, is often mis-regulated in disease and aging, how sFLT1 is trafficked ... ...

    Abstract FLT1/VEGFR1 negatively regulates VEGF-A signaling and is required for proper vessel morphogenesis during vascular development and vessel homeostasis. Although a soluble isoform, sFLT1, is often mis-regulated in disease and aging, how sFLT1 is trafficked and secreted from endothelial cells is not well understood. Here we define requirements for constitutive sFLT1 trafficking and secretion in endothelial cells from the Golgi to the plasma membrane, and we show that sFLT1 secretion requires clathrin at or near the Golgi. Perturbations that affect sFLT1 trafficking blunted endothelial cell secretion and promoted intracellular mis-localization in cells and zebrafish embryos. siRNA-mediated depletion of specific trafficking components revealed requirements for RAB27A, VAMP3, and STX3 for post-Golgi vesicle trafficking and sFLT1 secretion, while STX6, ARF1, and AP1 were required at the Golgi. Live-imaging of temporally controlled sFLT1 release from the endoplasmic reticulum showed clathrin-dependent sFLT1 trafficking at the Golgi into secretory vesicles that then trafficked to the plasma membrane. Depletion of STX6 altered vessel sprouting in 3D, suggesting that endothelial cell sFLT1 secretion influences proper vessel sprouting. Thus, specific trafficking components provide a secretory path from the Golgi to the plasma membrane for sFLT1 in endothelial cells that utilizes a specialized clathrin-dependent intermediate, suggesting novel therapeutic targets.
    MeSH term(s) Animals ; Endothelial Cells/metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism ; Clathrin/metabolism ; Zebrafish/metabolism
    Chemical Substances FLT1 protein, human (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-1 (EC 2.7.10.1) ; Clathrin
    Language English
    Publishing date 2023-09-11
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1484717-6
    ISSN 1573-7209 ; 0969-6970
    ISSN (online) 1573-7209
    ISSN 0969-6970
    DOI 10.1007/s10456-023-09893-6
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5094: Show issues Location:
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  9. Book: Collateral growth: role of Thymosin B4 and Notch

    Le Noble, Ferdinand

    Standortprojekt/Säule A/Säule B/Säule C: Säule B ; Laufzeit des Projektes: 01.01.2013 - 30.06.2014

    2013  

    Author's details [Autor Bericht]/Projektleiter: Ferdinand le Noble
    Language English
    Size 4 Bl.
    Publisher Max Delbrueck Center for Molecular Medicine (MDC)
    Publishing place Berlin
    Document type Book
    Note Förderkennzeichen BMU 81X2100104 ; Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  10. Article ; Online: Editorial Expression of Concern: The netrin receptor UNC5B mediates guidance events controlling morphogenesis of the vascular system.

    Lu, Xiaowei / le Noble, Ferdinand / Yuan, Li / Jiang, Quingjan / de Lafarge, Benjamin / Sugiyama, Daisuke / Bréant, Christiane / Claes, Filip / De Smet, Frederik / Thomas, Jean- Léon / Autiero, Monica / Carmeliet, Peter / Tessier-Lavigne, Marc / Eichmann, Anne

    Nature

    2023  Volume 625, Issue 7994, Page(s) E12

    Language English
    Publishing date 2023-12-18
    Publishing country England
    Document type Expression of Concern
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-06944-2
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    Zs.MG 9: Show issues
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