LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 102

Search options

  1. Article ; Online: The Beauty and Complexity of Blood Vessel Patterning.

    Bautch, Victoria L / Mukouyama, Yoh-Suke

    Cold Spring Harbor perspectives in medicine

    2022  Volume 12, Issue 11

    Abstract: This review highlights new concepts in vascular patterning in the last 10 years, with emphasis on its beauty and complexity. Endothelial cell signaling pathways that respond to molecular or mechanical signals are described, and examples of vascular ... ...

    Abstract This review highlights new concepts in vascular patterning in the last 10 years, with emphasis on its beauty and complexity. Endothelial cell signaling pathways that respond to molecular or mechanical signals are described, and examples of vascular patterning that use these pathways in brain, skin, heart, and kidney are highlighted. The pathological consequences of patterning loss are discussed in the context of arteriovenous malformations (AVMs), and prospects for the next 10 years presented.
    MeSH term(s) Humans ; Arteriovenous Malformations/metabolism ; Arteriovenous Malformations/pathology ; Signal Transduction ; Brain/metabolism
    Language English
    Publishing date 2022-11-01
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a041167
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: New plugs for CCM bleeds.

    Bautch, Victoria L

    Blood

    2019  Volume 133, Issue 3, Page(s) 183–184

    MeSH term(s) Animals ; Anticoagulants ; Hemangioma, Cavernous, Central Nervous System ; Hemorrhage ; Humans ; Mice
    Chemical Substances Anticoagulants
    Language English
    Publishing date 2019-01-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-11-887539
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Bone morphogenetic protein and blood vessels: new insights into endothelial cell junction regulation.

    Bautch, Victoria L

    Current opinion in hematology

    2019  Volume 26, Issue 3, Page(s) 154–160

    Abstract: Purpose of review: BMP signaling is an important regulator of vascular development and homeostasis, and perturbations of BMP pathway components are linked to vascular disease. However, until recently BMP's broad requirements in many developmental ... ...

    Abstract Purpose of review: BMP signaling is an important regulator of vascular development and homeostasis, and perturbations of BMP pathway components are linked to vascular disease. However, until recently BMP's broad requirements in many developmental programs delayed cause-and-effect and mechanistic studies of its vascular role in vivo. This review covers recent findings that illuminate the role of BMP signaling in endothelial cells of blood vessels, and highlights effects of BMP signaling on endothelial cell junctions and vascular barrier function.
    Recent findings: BMP signaling in endothelial cells of blood vessels is context-dependent, and can either be pro-angiogenic and promote vascular sprouting, or antiangiogenic and promote vascular homeostasis. I discuss how distinct BMP signaling inputs impact blood vessel formation and function, with emphasis on new studies that investigate how BMP signaling affects endothelial cell junctions and vascular permeability.
    Summary: BMP signaling is important but complex in endothelial cells of blood vessels, with multiple distinct inputs leading to opposing cellular behaviors and phenotypic outputs in ways that are poorly understood. Endothelial cell-cell junctions are a target of BMP signaling, and junction stability can be tuned in either direction by BMP inputs. Several human diseases have perturbed junctions linked to BMP signaling changes.
    MeSH term(s) Animals ; Blood Vessels/metabolism ; Bone Morphogenetic Proteins/metabolism ; Endothelial Cells/metabolism ; Humans ; Intercellular Junctions/metabolism ; Signal Transduction
    Chemical Substances Bone Morphogenetic Proteins
    Language English
    Publishing date 2019-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000492
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Endoglin moves and shapes endothelial cells.

    Bautch, Victoria L

    Nature cell biology

    2017  Volume 19, Issue 6, Page(s) 593–595

    Abstract: Vascular malformations result from improper blood vessel responses to molecular and mechanical signals. Two studies now show that endothelial cell migration and cell shape changes are perturbed in mutants lacking the TGFβ/BMP co-receptor endoglin, ... ...

    Abstract Vascular malformations result from improper blood vessel responses to molecular and mechanical signals. Two studies now show that endothelial cell migration and cell shape changes are perturbed in mutants lacking the TGFβ/BMP co-receptor endoglin, leading to arteriovenous shunts. Endoglin coordinates endothelial cell responses to ligand-receptor signalling and flow-mediated mechanical cues.
    MeSH term(s) Animals ; Bone Morphogenetic Proteins/metabolism ; Cell Movement ; Cell Shape ; Endoglin/metabolism ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Humans ; Signal Transduction ; Transforming Growth Factor beta/metabolism
    Chemical Substances Bone Morphogenetic Proteins ; Endoglin ; Transforming Growth Factor beta
    Language English
    Publishing date 2017-05-31
    Publishing country England
    Document type Journal Article
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/ncb3543
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: The versatility and paradox of BMP signaling in endothelial cell behaviors and blood vessel function.

    Kulikauskas, Molly R / X, Shaka / Bautch, Victoria L

    Cellular and molecular life sciences : CMLS

    2022  Volume 79, Issue 2, Page(s) 77

    Abstract: Blood vessels expand via sprouting angiogenesis, and this process involves numerous endothelial cell behaviors, such as collective migration, proliferation, cell-cell junction rearrangements, and anastomosis and lumen formation. Subsequently, blood ... ...

    Abstract Blood vessels expand via sprouting angiogenesis, and this process involves numerous endothelial cell behaviors, such as collective migration, proliferation, cell-cell junction rearrangements, and anastomosis and lumen formation. Subsequently, blood vessels remodel to form a hierarchical network that circulates blood and delivers oxygen and nutrients to tissue. During this time, endothelial cells become quiescent and form a barrier between blood and tissues that regulates transport of liquids and solutes. Bone morphogenetic protein (BMP) signaling regulates both proangiogenic and homeostatic endothelial cell behaviors as blood vessels form and mature. Almost 30 years ago, human pedigrees linked BMP signaling to diseases associated with blood vessel hemorrhage and shunts, and recent work greatly expanded our knowledge of the players and the effects of vascular BMP signaling. Despite these gains, there remain paradoxes and questions, especially with respect to how and where the different and opposing BMP signaling outputs are regulated. This review examines endothelial cell BMP signaling in vitro and in vivo and discusses the paradox of BMP signals that both destabilize and stabilize endothelial cell behaviors.
    MeSH term(s) Animals ; Blood Vessels/physiology ; Bone Morphogenetic Proteins/metabolism ; Endothelial Cells/metabolism ; Humans ; Intercellular Junctions/metabolism ; Neovascularization, Physiologic ; Signal Transduction
    Chemical Substances Bone Morphogenetic Proteins
    Language English
    Publishing date 2022-01-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-04033-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article: Differential endothelial cell cycle status in postnatal retinal vessels revealed using a novel PIP-FUCCI reporter and zonation analysis.

    Liu, Ziqing / Tanke, Natalie T / Neal, Alexandra / Yu, Tianji / Branch, Tershona / Cook, Jean G / Bautch, Victoria L

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Cell cycle regulation is critical to blood vessel formation and function, but how the endothelial cell cycle integrates with vascular regulation is not well-understood, and available dynamic cell cycle reporters do not precisely distinguish all cell ... ...

    Abstract Cell cycle regulation is critical to blood vessel formation and function, but how the endothelial cell cycle integrates with vascular regulation is not well-understood, and available dynamic cell cycle reporters do not precisely distinguish all cell cycle stage transitions
    Language English
    Publishing date 2024-01-05
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.04.574239
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Trafficking dynamics of VEGFR1, VEGFR2, and NRP1 in human endothelial cells.

    Sarabipour, Sarvenaz / Kinghorn, Karina / Quigley, Kaitlyn M / Kovacs-Kasa, Anita / Annex, Brian H / Bautch, Victoria L / Mac Gabhann, Feilim

    PLoS computational biology

    2024  Volume 20, Issue 2, Page(s) e1011798

    Abstract: The vascular endothelial growth factor (VEGF) family of cytokines are key drivers of blood vessel growth and remodeling. These ligands act via multiple VEGF receptors (VEGFR) and co-receptors such as Neuropilin (NRP) expressed on endothelial cells. These ...

    Abstract The vascular endothelial growth factor (VEGF) family of cytokines are key drivers of blood vessel growth and remodeling. These ligands act via multiple VEGF receptors (VEGFR) and co-receptors such as Neuropilin (NRP) expressed on endothelial cells. These membrane-associated receptors are not solely expressed on the cell surface, they move between the surface and intracellular locations, where they can function differently. The location of the receptor alters its ability to 'see' (access and bind to) its ligands, which regulates receptor activation; location also alters receptor exposure to subcellularly localized phosphatases, which regulates its deactivation. Thus, receptors in different subcellular locations initiate different signaling, both in terms of quantity and quality. Similarly, the local levels of co-expression of other receptors alters competition for ligands. Subcellular localization is controlled by intracellular trafficking processes, which thus control VEGFR activity; therefore, to understand VEGFR activity, we must understand receptor trafficking. Here, for the first time, we simultaneously quantify the trafficking of VEGFR1, VEGFR2, and NRP1 on the same cells-specifically human umbilical vein endothelial cells (HUVECs). We build a computational model describing the expression, interaction, and trafficking of these receptors, and use it to simulate cell culture experiments. We use new quantitative experimental data to parameterize the model, which then provides mechanistic insight into the trafficking and localization of this receptor network. We show that VEGFR2 and NRP1 trafficking is not the same on HUVECs as on non-human ECs; and we show that VEGFR1 trafficking is not the same as VEGFR2 trafficking, but rather is faster in both internalization and recycling. As a consequence, the VEGF receptors are not evenly distributed between the cell surface and intracellular locations, with a very low percentage of VEGFR1 being on the cell surface, and high levels of NRP1 on the cell surface. Our findings have implications both for the sensing of extracellular ligands and for the composition of signaling complexes at the cell surface versus inside the cell.
    MeSH term(s) Humans ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Signal Transduction ; Phosphorylation ; Neuropilin-1/metabolism
    Chemical Substances Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1 (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; Neuropilin-1 (144713-63-3)
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2193340-6
    ISSN 1553-7358 ; 1553-734X
    ISSN (online) 1553-7358
    ISSN 1553-734X
    DOI 10.1371/journal.pcbi.1011798
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Endothelial Cell SMAD6 Balances ACVRL1/Alk1 Function to Regulate Adherens Junctions and Hepatic Vascular Development.

    Kulikauskas, Molly R / Oatley, Morgan / Yu, Tianji / Liu, Ziqing / Matsumura, Lauren / Kidder, Elise / Ruter, Dana / Bautch, Victoria L

    bioRxiv : the preprint server for biology

    2023  

    Abstract: BMP signaling is critical to blood vessel formation and function, but how pathway components regulate vascular development is not well-understood. Here we find that inhibitory SMAD6 functions in endothelial cells to negatively regulate ALK1/ACVRL1- ... ...

    Abstract BMP signaling is critical to blood vessel formation and function, but how pathway components regulate vascular development is not well-understood. Here we find that inhibitory SMAD6 functions in endothelial cells to negatively regulate ALK1/ACVRL1-mediated responses, and it is required to prevent vessel dysmorphogenesis and hemorrhage in the embryonic liver vasculature. Reduced
    Language English
    Publishing date 2023-03-25
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.03.23.534007
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article: The versatility and paradox of BMP signaling in endothelial cell behaviors and blood vessel function

    Kulikauskas, Molly R. / X, Shaka / Bautch, Victoria L.

    Cellular and molecular life sciences. 2022 Feb., v. 79, no. 2

    2022  

    Abstract: Blood vessels expand via sprouting angiogenesis, and this process involves numerous endothelial cell behaviors, such as collective migration, proliferation, cell–cell junction rearrangements, and anastomosis and lumen formation. Subsequently, blood ... ...

    Abstract Blood vessels expand via sprouting angiogenesis, and this process involves numerous endothelial cell behaviors, such as collective migration, proliferation, cell–cell junction rearrangements, and anastomosis and lumen formation. Subsequently, blood vessels remodel to form a hierarchical network that circulates blood and delivers oxygen and nutrients to tissue. During this time, endothelial cells become quiescent and form a barrier between blood and tissues that regulates transport of liquids and solutes. Bone morphogenetic protein (BMP) signaling regulates both proangiogenic and homeostatic endothelial cell behaviors as blood vessels form and mature. Almost 30 years ago, human pedigrees linked BMP signaling to diseases associated with blood vessel hemorrhage and shunts, and recent work greatly expanded our knowledge of the players and the effects of vascular BMP signaling. Despite these gains, there remain paradoxes and questions, especially with respect to how and where the different and opposing BMP signaling outputs are regulated. This review examines endothelial cell BMP signaling in vitro and in vivo and discusses the paradox of BMP signals that both destabilize and stabilize endothelial cell behaviors.
    Keywords angiogenesis ; blood ; blood vessels ; bone morphogenetic proteins ; endothelial cells ; hemorrhage ; humans ; oxygen
    Language English
    Dates of publication 2022-02
    Size p. 77.
    Publishing place Springer International Publishing
    Document type Article
    Note Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-04033-z
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

  10. Article ; Online: Endothelial cell SMAD6 balances Alk1 function to regulate adherens junctions and hepatic vascular development.

    Kulikauskas, Molly R / Oatley, Morgan / Yu, Tianji / Liu, Ziqing / Matsumura, Lauren / Kidder, Elise / Ruter, Dana / Bautch, Victoria L

    Development (Cambridge, England)

    2023  Volume 150, Issue 21

    Abstract: BMP signaling is crucial to blood vessel formation and function, but how pathway components regulate vascular development is not well-understood. Here, we find that inhibitory SMAD6 functions in endothelial cells to negatively regulate ALK1-mediated ... ...

    Abstract BMP signaling is crucial to blood vessel formation and function, but how pathway components regulate vascular development is not well-understood. Here, we find that inhibitory SMAD6 functions in endothelial cells to negatively regulate ALK1-mediated responses, and it is required to prevent vessel dysmorphogenesis and hemorrhage in the embryonic liver vasculature. Reduced Alk1 gene dosage rescued embryonic hepatic hemorrhage and microvascular capillarization induced by Smad6 deletion in endothelial cells in vivo. At the cellular level, co-depletion of Smad6 and Alk1 rescued the destabilized junctions and impaired barrier function of endothelial cells depleted for SMAD6 alone. Mechanistically, blockade of actomyosin contractility or increased PI3K signaling rescued endothelial junction defects induced by SMAD6 loss. Thus, SMAD6 normally modulates ALK1 function in endothelial cells to regulate PI3K signaling and contractility, and SMAD6 loss increases signaling through ALK1 that disrupts endothelial cell junctions. ALK1 loss-of-function also disrupts vascular development and function, indicating that balanced ALK1 signaling is crucial for proper vascular development and identifying ALK1 as a 'Goldilocks' pathway in vascular biology that requires a certain signaling amplitude, regulated by SMAD6, to function properly.
    MeSH term(s) Humans ; Adherens Junctions/metabolism ; Endothelial Cells/metabolism ; Hemorrhage/metabolism ; Liver/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Smad6 Protein/metabolism
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Smad6 Protein ; SMAD6 protein, human ; ACVRL1 protein, human (EC 2.7.11.30)
    Language English
    Publishing date 2023-11-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.201811
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top