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  1. AU="Carmen Ruiz de Almodóvar"
  2. AU="Qiu, Xudong"
  3. AU="Groh, M"
  4. AU="Defres, S"
  5. AU="Khurana, Navneet"
  6. AU="Yanshan Yang"
  7. AU=Brouillet Emmanuel AU=Brouillet Emmanuel
  8. AU="Rajput, Sandeep"
  9. AU="Mansfield, Shawn D"
  10. AU="Isolan, Cecilia"
  11. AU="Li, Yiran"
  12. AU="Kang, Weechang"
  13. AU="Landoni, Elisa"
  14. AU=McCubbin Keith I AU=McCubbin Keith I
  15. AU="Jessica Bijsterbosch"
  16. AU="Dela Cruz, Charles S."
  17. AU="Yoo, Jennifer"
  18. AU="Berger, Miriam B"
  19. AU="Carlson, Jeffrey R"

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  1. Artikel ; Online: Malaria parasites differentially sense environmental elasticity during transmission

    Johanna Ripp / Jessica Kehrer / Xanthoula Smyrnakou / Nathalie Tisch / Joana Tavares / Rogerio Amino / Carmen Ruiz de Almodovar / Friedrich Frischknecht

    EMBO Molecular Medicine, Vol 13, Iss 4, Pp n/a-n/a (2021)

    2021  

    Abstract: Abstract Transmission of malaria‐causing parasites to and by the mosquito relies on active parasite migration and constitutes bottlenecks in the Plasmodium life cycle. Parasite adaption to the biochemically and physically different environments must ... ...

    Abstract Abstract Transmission of malaria‐causing parasites to and by the mosquito relies on active parasite migration and constitutes bottlenecks in the Plasmodium life cycle. Parasite adaption to the biochemically and physically different environments must hence be a key evolutionary driver for transmission efficiency. To probe how subtle but physiologically relevant changes in environmental elasticity impact parasite migration, we introduce 2D and 3D polyacrylamide gels to study ookinetes, the parasite forms emigrating from the mosquito blood meal and sporozoites, the forms transmitted to the vertebrate host. We show that ookinetes adapt their migratory path but not their speed to environmental elasticity and are motile for over 24 h on soft substrates. In contrast, sporozoites evolved more short‐lived rapid gliding motility for rapidly crossing the skin. Strikingly, sporozoites are highly sensitive to substrate elasticity possibly to avoid adhesion to soft endothelial cells on their long way to the liver. Hence, the two migratory stages of Plasmodium evolved different strategies to overcome the physical challenges posed by the respective environments and barriers they encounter.
    Schlagwörter cell migration ; ookinete ; sporozoite ; substrate elasticity ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2021-04-01T00:00:00Z
    Verlag Wiley
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Protein Phosphatase 2A Mediates YAP Activation in Endothelial Cells Upon VEGF Stimulation and Matrix Stiffness

    Xiao Jiang / Jiandong Hu / Ziru Wu / Sarah Trusso Cafarello / Mario Di Matteo / Ying Shen / Xue Dong / Heike Adler / Massimiliano Mazzone / Carmen Ruiz de Almodovar / Xiaohong Wang

    Frontiers in Cell and Developmental Biology, Vol

    2021  Band 9

    Abstract: Angiogenesis is an essential process during development. Abnormal angiogenesis also contributes to many disease conditions such as tumor and retinal diseases. Previous studies have established the Hippo signaling pathway effector Yes-associated protein ( ... ...

    Abstract Angiogenesis is an essential process during development. Abnormal angiogenesis also contributes to many disease conditions such as tumor and retinal diseases. Previous studies have established the Hippo signaling pathway effector Yes-associated protein (YAP) as a crucial regulator of angiogenesis. In ECs, activated YAP promotes endothelial cell proliferation, migration and sprouting. YAP activity is regulated by vascular endothelial growth factor (VEGF) and mechanical cues such as extracellular matrix (ECM) stiffness. However, it is unclear how VEGF or ECM stiffness signal to YAP, especially how dephosphorylation of YAP occurs in response to VEGF stimulus or ECM stiffening. Here, we show that protein phosphatase 2A (PP2A) is required for this process. Blocking PP2A activity abolishes VEGF or ECM stiffening mediated YAP activation. Systemic administration of a PP2A inhibitor suppresses YAP activity in blood vessels in developmental and pathological angiogenesis mouse models. Consistently, PP2A inhibitor also inhibits sprouting angiogenesis. Mechanistically, PP2A directly interacts with YAP, and this interaction requires proper cytoskeleton dynamics. These findings identify PP2A as a crucial mediator of YAP activation in ECs and hence as an important regulator of angiogenesis.
    Schlagwörter angiogenesis ; YAP ; PP2A ; VEGF ; matrix stiffness ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2021-05-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Caspase‐8 in endothelial cells maintains gut homeostasis and prevents small bowel inflammation in mice

    Nathalie Tisch / Carolin Mogler / Ana Stojanovic / Robert Luck / Emilia A Korhonen / Alexander Ellerkmann / Heike Adler / Mahak Singhal / Géza Schermann / Lena Erkert / Jay V Patankar / Andromachi Karakatsani / Anna‐Lena Scherr / Yaron Fuchs / Adelheid Cerwenka / Stefan Wirtz / Bruno Christian Köhler / Hellmut G Augustin / Christoph Becker /
    Thomas Schmidt / Carmen Ruiz de Almodóvar

    EMBO Molecular Medicine, Vol 14, Iss 6, Pp n/a-n/a (2022)

    2022  

    Abstract: Abstract The gut has a specific vascular barrier that controls trafficking of antigens and microbiota into the bloodstream. However, the molecular mechanisms regulating the maintenance of this vascular barrier remain elusive. Here, we identified Caspase‐ ... ...

    Abstract Abstract The gut has a specific vascular barrier that controls trafficking of antigens and microbiota into the bloodstream. However, the molecular mechanisms regulating the maintenance of this vascular barrier remain elusive. Here, we identified Caspase‐8 as a pro‐survival factor in mature intestinal endothelial cells that is required to actively maintain vascular homeostasis in the small intestine in an organ‐specific manner. In particular, we find that deletion of Caspase‐8 in endothelial cells results in small intestinal hemorrhages and bowel inflammation, while all other organs remained unaffected. We also show that Caspase‐8 seems to be particularly needed in lymphatic endothelial cells to maintain gut homeostasis. Our work demonstrates that endothelial cell dysfunction, leading to the breakdown of the gut‐vascular barrier, is an active driver of chronic small intestinal inflammation, highlighting the role of the intestinal vasculature as a safeguard of organ function.
    Schlagwörter caspase‐8 ; chronic intestinal inflammation ; endothelium ; necroptosis ; vascular homeostasis ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-06-01T00:00:00Z
    Verlag Wiley
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: EphrinB2 regulates VEGFR2 during dendritogenesis and hippocampal circuitry development

    Eva Harde / LaShae Nicholson / Beatriz Furones Cuadrado / Diane Bissen / Sylvia Wigge / Severino Urban / Marta Segarra / Carmen Ruiz de Almodóvar / Amparo Acker-Palmer

    eLife, Vol

    2019  Band 8

    Abstract: Vascular endothelial growth factor (VEGF) is an angiogenic factor that play important roles in the nervous system, although it is still unclear which receptors transduce those signals in neurons. Here, we show that in the developing hippocampus VEGFR2 ( ... ...

    Abstract Vascular endothelial growth factor (VEGF) is an angiogenic factor that play important roles in the nervous system, although it is still unclear which receptors transduce those signals in neurons. Here, we show that in the developing hippocampus VEGFR2 (also known as KDR or FLK1) is expressed specifically in the CA3 region and it is required for dendritic arborization and spine morphogenesis in hippocampal neurons. Mice lacking VEGFR2 in neurons (Nes-cre Kdrlox/-) show decreased dendritic arbors and spines as well as a reduction in long-term potentiation (LTP) at the associational-commissural – CA3 synapses. Mechanistically, VEGFR2 internalization is required for VEGF-induced spine maturation. In analogy to endothelial cells, ephrinB2 controls VEGFR2 internalization in neurons. VEGFR2-ephrinB2 compound mice (Nes-cre Kdrlox/+ Efnb2lox/+) show reduced dendritic branching, reduced spine head size and impaired LTP. Our results demonstrate the functional crosstalk of VEGFR2 and ephrinB2 in vivo to control dendritic arborization, spine morphogenesis and hippocampal circuitry development.
    Schlagwörter hippocampal development ; neurovascular link ; dendritic arborisation ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2019-12-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: VEGF/VEGFR2 signaling regulates hippocampal axon branching during development

    Robert Luck / Severino Urban / Andromachi Karakatsani / Eva Harde / Sivakumar Sambandan / LaShae Nicholson / Silke Haverkamp / Rebecca Mann / Ana Martin-Villalba / Erin Margaret Schuman / Amparo Acker-Palmer / Carmen Ruiz de Almodóvar

    eLife, Vol

    2019  Band 8

    Abstract: Axon branching is crucial for proper formation of neuronal networks. Although originally identified as an angiogenic factor, VEGF also signals directly to neurons to regulate their development and function. Here we show that VEGF and its receptor VEGFR2 ( ...

    Abstract Axon branching is crucial for proper formation of neuronal networks. Although originally identified as an angiogenic factor, VEGF also signals directly to neurons to regulate their development and function. Here we show that VEGF and its receptor VEGFR2 (also known as KDR or FLK1) are expressed in mouse hippocampal neurons during development, with VEGFR2 locally expressed in the CA3 region. Activation of VEGF/VEGFR2 signaling in isolated hippocampal neurons results in increased axon branching. Remarkably, inactivation of VEGFR2 also results in increased axon branching in vitro and in vivo. The increased CA3 axon branching is not productive as these axons are less mature and form less functional synapses with CA1 neurons. Mechanistically, while VEGF promotes the growth of formed branches without affecting filopodia formation, loss of VEGFR2 increases the number of filopodia and enhances the growth rate of new branches. Thus, a controlled VEGF/VEGFR2 signaling is required for proper CA3 hippocampal axon branching during mouse hippocampus development.
    Schlagwörter develomental neuroscience ; axon branching ; neuro-vascular link ; VEGF ; VEGFR2 ; hippocampus ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2019-12-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: VEGF ligands and receptors: implications in neurodevelopment and neurodegeneration.

    Carmeliet, Peter / Ruiz de Almodovar, Carmen / Carmen, Ruiz de Almodovar

    Cellular and molecular life sciences : CMLS

    2013  Band 70, Heft 10, Seite(n) 1763–1778

    Abstract: Intensive research in the last decade shows that the prototypic angiogenic factor vascular endothelial growth factor (VEGF) can have direct effects in neurons and modulate processes such as neuronal migration, axon outgrowth, axon guidance and neuronal ... ...

    Abstract Intensive research in the last decade shows that the prototypic angiogenic factor vascular endothelial growth factor (VEGF) can have direct effects in neurons and modulate processes such as neuronal migration, axon outgrowth, axon guidance and neuronal survival. Depending on the neuronal cell type and the process, VEGF seems to exert these effects by signaling via different receptors. It is also becoming clear that other VEGF ligands such as VEGF-B, -C and -D can act in various neuronal cell types as well. Moreover, apart from playing a role in physiological conditions, VEGF and VEGF-B have been related to different neurological disorders. We give an update on how VEGF controls different processes during neurodevelopment as well as on its role in several neurodegenerative disorders. We also discuss recent findings demonstrating that other VEGF ligands influence processes such as neurogenesis and dendrite arborization and participate in neurodegeneration.
    Mesh-Begriff(e) Animals ; Cell Movement ; Dendrites/metabolism ; Humans ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neurogenesis ; Neurons/cytology ; Neurons/metabolism ; Peripheral Nervous System/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism
    Chemische Substanzen Protein Isoforms ; Vascular Endothelial Growth Factor A ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2013-03-12
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-013-1283-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Motor neurons control blood vessel patterning in the developing spinal cord

    Patricia Himmels / Isidora Paredes / Heike Adler / Andromachi Karakatsani / Robert Luck / Hugo H. Marti / Olga Ermakova / Eugen Rempel / Esther T. Stoeckli / Carmen Ruiz de Almodóvar

    Nature Communications, Vol 8, Iss 1, Pp 1-

    2017  Band 16

    Abstract: The guidance cues regulating blood vessel patterning in the central nervous system remain unclear. Here, the authors show in mice and chicken developing spinal cord that motor neurons control blood vessel patterning by an autocrine mechanism titrating ... ...

    Abstract The guidance cues regulating blood vessel patterning in the central nervous system remain unclear. Here, the authors show in mice and chicken developing spinal cord that motor neurons control blood vessel patterning by an autocrine mechanism titrating VEGF via the expression of its trapping receptor sFlt1.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2017-03-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: CNS Macrophages Control Neurovascular Development via CD95L

    Si Chen / Nathalie Tisch / Marcel Kegel / Rosario Yerbes / Robert Hermann / Hannes Hudalla / Cecilia Zuliani / Gülce Sila Gülcüler / Klara Zwadlo / Jakob von Engelhardt / Carmen Ruiz de Almodóvar / Ana Martin-Villalba

    Cell Reports, Vol 19, Iss 7, Pp 1378-

    2017  Band 1393

    Abstract: The development of neurons and vessels shares striking anatomical and molecular features, and it is presumably orchestrated by an overlapping repertoire of extracellular signals. CNS macrophages have been implicated in various developmental functions, ... ...

    Abstract The development of neurons and vessels shares striking anatomical and molecular features, and it is presumably orchestrated by an overlapping repertoire of extracellular signals. CNS macrophages have been implicated in various developmental functions, including the morphogenesis of neurons and vessels. However, whether CNS macrophages can coordinately influence neurovascular development and the identity of the signals involved therein is unclear. Here, we demonstrate that activity of the cell surface receptor CD95 regulates neuronal and vascular morphogenesis in the post-natal brain and retina. Furthermore, we identify CNS macrophages as the main source of CD95L, and macrophage-specific deletion thereof reduces both neurovascular complexity and synaptic activity in the brain. CD95L-induced neuronal and vascular growth is mediated through src-family kinase (SFK) and PI3K signaling. Together, our study highlights a coordinated neurovascular development instructed by CNS macrophage-derived CD95L, and it underlines the importance of macrophages for the establishment of the neurovascular network during CNS development.
    Schlagwörter CNS macrophages ; microglia ; neurovascular development ; vessel ; angiogenesis ; CD95 ; CD95L ; cortex ; retina ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2017-05-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: A new mouse model to study acquired lymphedema.

    Martin Schneider / Annelii Ny / Carmen Ruiz de Almodovar / Peter Carmeliet

    PLoS Medicine, Vol 3, Iss 7, p e

    2006  Band 264

    Schlagwörter Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2006-07-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
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  10. Artikel ; Online: The Oxygen Sensor PHD2 Controls Dendritic Spines and Synapses via Modification of Filamin A

    Inmaculada Segura / Christian Lange / Ellen Knevels / Anastasiya Moskalyuk / Rocco Pulizzi / Guy Eelen / Thibault Chaze / Cicerone Tudor / Cyril Boulegue / Matthew Holt / Dirk Daelemans / Mariette Matondo / Bart Ghesquière / Michele Giugliano / Carmen Ruiz de Almodovar / Mieke Dewerchin / Peter Carmeliet

    Cell Reports, Vol 14, Iss 11, Pp 2653-

    2016  Band 2667

    Abstract: Neuronal function is highly sensitive to changes in oxygen levels, but how hypoxia affects dendritic spine formation and synaptogenesis is unknown. Here we report that hypoxia, chemical inhibition of the oxygen-sensing prolyl hydroxylase domain proteins ( ...

    Abstract Neuronal function is highly sensitive to changes in oxygen levels, but how hypoxia affects dendritic spine formation and synaptogenesis is unknown. Here we report that hypoxia, chemical inhibition of the oxygen-sensing prolyl hydroxylase domain proteins (PHDs), and silencing of Phd2 induce immature filopodium-like dendritic protrusions, promote spine regression, reduce synaptic density, and decrease the frequency of spontaneous action potentials independently of HIF signaling. We identified the actin cross-linker filamin A (FLNA) as a target of PHD2 mediating these effects. In normoxia, PHD2 hydroxylates the proline residues P2309 and P2316 in FLNA, leading to von Hippel-Lindau (VHL)-mediated ubiquitination and proteasomal degradation. In hypoxia, PHD2 inactivation rapidly upregulates FLNA protein levels because of blockage of its proteasomal degradation. FLNA upregulation induces more immature spines, whereas Flna silencing rescues the immature spine phenotype induced by PHD2 inhibition.
    Schlagwörter Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2016-03-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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