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  1. Artikel ; Online: Eating your own fat to stay fit: lipophagy sustains lymphangiogenesis.

    Mece, Odeta / Houbaert, Diede / Agostinis, Patrizia

    Autophagy

    2022  Band 19, Heft 4, Seite(n) 1351–1353

    Abstract: Lymphatic endothelial cells (LECs) exploit fatty acid oxidation (FAO) to grow and to maintain lymphatic vessel identity through the epigenetic regulation of the essential transcription factor PROX1. In our recent study, we found that LEC-specific loss ... ...

    Abstract Lymphatic endothelial cells (LECs) exploit fatty acid oxidation (FAO) to grow and to maintain lymphatic vessel identity through the epigenetic regulation of the essential transcription factor PROX1. In our recent study, we found that LEC-specific loss of
    Mesh-Begriff(e) Mice ; Animals ; Lymphangiogenesis ; Endothelial Cells/metabolism ; Epigenesis, Genetic ; Acetyl Coenzyme A/metabolism ; Homeodomain Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Autophagy ; Inflammation/metabolism ; Mice, Knockout ; Fatty Acids/metabolism
    Chemische Substanzen Acetyl Coenzyme A (72-89-9) ; Homeodomain Proteins ; Tumor Suppressor Proteins ; Fatty Acids
    Sprache Englisch
    Erscheinungsdatum 2022-09-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2117513
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Autophagy in endothelial cells and tumor angiogenesis.

    Schaaf, Marco B / Houbaert, Diede / Meçe, Odeta / Agostinis, Patrizia

    Cell death and differentiation

    2019  Band 26, Heft 4, Seite(n) 665–679

    Abstract: In mammalian cells, autophagy is the major pathway for the degradation and recycling of obsolete and potentially noxious cytoplasmic materials, including proteins, lipids, and whole organelles, through the lysosomes. Autophagy maintains cellular and ... ...

    Abstract In mammalian cells, autophagy is the major pathway for the degradation and recycling of obsolete and potentially noxious cytoplasmic materials, including proteins, lipids, and whole organelles, through the lysosomes. Autophagy maintains cellular and tissue homeostasis and provides a mechanism to adapt to extracellular cues and metabolic stressors. Emerging evidence unravels a critical function of autophagy in endothelial cells (ECs), the major components of the blood vasculature, which delivers nutrients and oxygen to the parenchymal tissue. EC-intrinsic autophagy modulates the response of ECs to various metabolic stressors and has a fundamental role in redox homeostasis and EC plasticity. In recent years moreover, genetic evidence suggests that autophagy regulates pathological angiogenesis, a hallmark of solid tumors. In the hypoxic, nutrient-deprived, and pro-angiogenic tumor microenvironment, heightened autophagy in the blood vessels is emerging as a critical mechanism enabling ECs to dynamically accommodate their higher bioenergetics demands to the extracellular environment and connect with other components of the tumor stroma through paracrine signaling. In this review, we provide an overview of the major cellular mechanisms regulated by autophagy in ECs and discuss their potential role in tumor angiogenesis, tumor growth, and response to anticancer therapy.
    Mesh-Begriff(e) Animals ; Autophagy/genetics ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Lipid Metabolism/genetics ; Lysosomes/genetics ; Lysosomes/metabolism ; Neoplasms/blood ; Neoplasms/metabolism ; Neovascularization, Pathologic/metabolism ; Oxidation-Reduction ; Paracrine Communication/genetics ; Paracrine Communication/physiology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Signal Transduction/physiology ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
    Sprache Englisch
    Erscheinungsdatum 2019-01-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-019-0287-8
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: An autophagy program that promotes T cell egress from the lymph node controls responses to immune checkpoint blockade.

    Houbaert, Diede / Nikolakopoulos, Apostolos Panagiotis / Jacobs, Kathryn A / Meçe, Odeta / Roels, Jana / Shankar, Gautam / Agrawal, Madhur / More, Sanket / Ganne, Maarten / Rillaerts, Kristine / Boon, Louis / Swoboda, Magdalena / Nobis, Max / Mourao, Larissa / Bosisio, Francesca / Vandamme, Niels / Bergers, Gabriele / Scheele, Colinda L G J / Agostinis, Patrizia

    Cell reports

    2024  Band 43, Heft 4, Seite(n) 114020

    Abstract: Lymphatic endothelial cells (LECs) of the lymph node (LN) parenchyma orchestrate leukocyte trafficking and peripheral T cell dynamics. T cell responses to immunotherapy largely rely on peripheral T cell recruitment in tumors. Yet, a systematic and ... ...

    Abstract Lymphatic endothelial cells (LECs) of the lymph node (LN) parenchyma orchestrate leukocyte trafficking and peripheral T cell dynamics. T cell responses to immunotherapy largely rely on peripheral T cell recruitment in tumors. Yet, a systematic and molecular understanding of how LECs within the LNs control T cell dynamics under steady-state and tumor-bearing conditions is lacking. Intravital imaging combined with immune phenotyping shows that LEC-specific deletion of the essential autophagy gene Atg5 alters intranodal positioning of lymphocytes and accrues their persistence in the LNs by increasing the availability of the main egress signal sphingosine-1-phosphate. Single-cell RNA sequencing of tumor-draining LNs shows that loss of ATG5 remodels niche-specific LEC phenotypes involved in molecular pathways regulating lymphocyte trafficking and LEC-T cell interactions. Functionally, loss of LEC autophagy prevents recruitment of tumor-infiltrating T and natural killer cells and abrogates response to immunotherapy. Thus, an LEC-autophagy program boosts immune-checkpoint responses by guiding systemic T cell dynamics.
    Mesh-Begriff(e) Autophagy/drug effects ; Animals ; Lymph Nodes/immunology ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Mice ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Mice, Inbred C57BL ; Autophagy-Related Protein 5/metabolism ; Autophagy-Related Protein 5/genetics ; Endothelial Cells/metabolism ; Sphingosine/analogs & derivatives ; Sphingosine/pharmacology ; Sphingosine/metabolism ; Humans ; Lysophospholipids/metabolism ; Immunotherapy/methods ; Cell Movement
    Chemische Substanzen Immune Checkpoint Inhibitors ; Autophagy-Related Protein 5 ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine (NGZ37HRE42) ; Lysophospholipids ; Atg5 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2024-03-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.114020
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Lysosomal Pathways and Autophagy Distinctively Control Endothelial Cell Behavior to Affect Tumor Vasculature.

    Schaaf, Marco B / Houbaert, Diede / Meçe, Odeta / To, San Kit / Ganne, Maarten / Maes, Hannelore / Agostinis, Patrizia

    Frontiers in oncology

    2019  Band 9, Seite(n) 171

    Abstract: Cancer cell-stromal cell crosstalk is orchestrated by a plethora of ligand-receptor interactions generating a tumor microenvironment (TME) which favors tumor growth. The high pro-angiogenic nature of the TME perpetuates the chaotic network of ... ...

    Abstract Cancer cell-stromal cell crosstalk is orchestrated by a plethora of ligand-receptor interactions generating a tumor microenvironment (TME) which favors tumor growth. The high pro-angiogenic nature of the TME perpetuates the chaotic network of structurally immature, low pericyte-covered vessels characteristic of the tumor vasculature. We previously demonstrated that chloroquine (CQ) -a lysosomotropic agent used as first-generation autophagy blocker in clinical trials- induced tumor vessel normalization and reduced tumor hypoxia. CQ improved both vessel structure and maturation, whereas the conditional knockout of the crucial autophagy gene
    Sprache Englisch
    Erscheinungsdatum 2019-03-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2019.00171
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Tumor endothelial cell autophagy is a key vascular-immune checkpoint in melanoma.

    Verhoeven, Jelle / Jacobs, Kathryn A / Rizzollo, Francesca / Lodi, Francesca / Hua, Yichao / Poźniak, Joanna / Narayanan Srinivasan, Adhithya / Houbaert, Diede / Shankar, Gautam / More, Sanket / Schaaf, Marco B / Dubroja Lakic, Nikolina / Ganne, Maarten / Lamote, Jochen / Van Weyenbergh, Johan / Boon, Louis / Bechter, Oliver / Bosisio, Francesca / Uchiyama, Yasuo /
    Bertrand, Mathieu Jm / Marine, Jean Christophe / Lambrechts, Diether / Bergers, Gabriele / Agrawal, Madhur / Agostinis, Patrizia

    EMBO molecular medicine

    2023  Band 15, Heft 12, Seite(n) e18028

    Abstract: Tumor endothelial cells (TECs) actively repress inflammatory responses and maintain an immune-excluded tumor phenotype. However, the molecular mechanisms that sustain TEC-mediated immunosuppression remain largely elusive. Here, we show that autophagy ... ...

    Abstract Tumor endothelial cells (TECs) actively repress inflammatory responses and maintain an immune-excluded tumor phenotype. However, the molecular mechanisms that sustain TEC-mediated immunosuppression remain largely elusive. Here, we show that autophagy ablation in TECs boosts antitumor immunity by supporting infiltration and effector function of T-cells, thereby restricting melanoma growth. In melanoma-bearing mice, loss of TEC autophagy leads to the transcriptional expression of an immunostimulatory/inflammatory TEC phenotype driven by heightened NF-kB and STING signaling. In line, single-cell transcriptomic datasets from melanoma patients disclose an enriched Inflammatory
    Mesh-Begriff(e) Humans ; Mice ; Animals ; Melanoma/pathology ; Endothelial Cells/metabolism ; CD8-Positive T-Lymphocytes ; NF-kappa B/metabolism ; Autophagy ; Immunotherapy ; Tumor Microenvironment
    Chemische Substanzen NF-kappa B
    Sprache Englisch
    Erscheinungsdatum 2023-11-27
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202318028
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6784: Hefte anzeigen Standort:
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  6. Artikel ; Online: Lipid droplet degradation by autophagy connects mitochondria metabolism to Prox1-driven expression of lymphatic genes and lymphangiogenesis.

    Meçe, Odeta / Houbaert, Diede / Sassano, Maria-Livia / Durré, Tania / Maes, Hannelore / Schaaf, Marco / More, Sanket / Ganne, Maarten / García-Caballero, Melissa / Borri, Mila / Verhoeven, Jelle / Agrawal, Madhur / Jacobs, Kathryn / Bergers, Gabriele / Blacher, Silvia / Ghesquière, Bart / Dewerchin, Mieke / Swinnen, Johan V / Vinckier, Stefan /
    Soengas, María S / Carmeliet, Peter / Noël, Agnès / Agostinis, Patrizia

    Nature communications

    2022  Band 13, Heft 1, Seite(n) 2760

    Abstract: Autophagy has vasculoprotective roles, but whether and how it regulates lymphatic endothelial cells (LEC) homeostasis and lymphangiogenesis is unknown. Here, we show that genetic deficiency of autophagy in LEC impairs responses to VEGF-C and injury- ... ...

    Abstract Autophagy has vasculoprotective roles, but whether and how it regulates lymphatic endothelial cells (LEC) homeostasis and lymphangiogenesis is unknown. Here, we show that genetic deficiency of autophagy in LEC impairs responses to VEGF-C and injury-driven corneal lymphangiogenesis. Autophagy loss in LEC compromises the expression of main effectors of LEC identity, like VEGFR3, affects mitochondrial dynamics and causes an accumulation of lipid droplets (LDs) in vitro and in vivo. When lipophagy is impaired, mitochondrial ATP production, fatty acid oxidation, acetyl-CoA/CoA ratio and expression of lymphangiogenic PROX1 target genes are dwindled. Enforcing mitochondria fusion by silencing dynamin-related-protein 1 (DRP1) in autophagy-deficient LEC fails to restore LDs turnover and lymphatic gene expression, whereas supplementing the fatty acid precursor acetate rescues VEGFR3 levels and signaling, and lymphangiogenesis in LEC-Atg5
    Mesh-Begriff(e) Animals ; Autophagy/genetics ; Endothelial Cells/metabolism ; Fatty Acids/metabolism ; Lipid Droplets/metabolism ; Lymphangiogenesis/genetics ; Lymphatic Vessels/metabolism ; Mice ; Mitochondria ; Transcription Factors/metabolism
    Chemische Substanzen Fatty Acids ; Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2022-05-19
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-30490-6
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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