LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 188

Search options

  1. Article ; Online: Introducing the Ocular Pathobiology Topic Category in The American Journal of Pathology.

    D'Amore, Patricia A

    The American journal of pathology

    2023  Volume 193, Issue 11, Page(s) 1620–1621

    MeSH term(s) United States ; Vision, Ocular ; Pathology, Clinical ; Face ; Pathology
    Language English
    Publishing date 2023-10-12
    Publishing country United States
    Document type Editorial
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2023.09.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Macrophage efferocytosis with VEGFC and lymphangiogenesis: rescuing the broken heart.

    D'Amore, Patricia A / Alcaide, Pilar

    The Journal of clinical investigation

    2022  Volume 132, Issue 9

    Abstract: Cardiac repair following ischemic injury is indispensable for survival and requires a coordinated cellular response involving the mobilization of immune cells from the secondary lymphoid organs to the site of damage. Efferocytosis, the engulfment of cell ...

    Abstract Cardiac repair following ischemic injury is indispensable for survival and requires a coordinated cellular response involving the mobilization of immune cells from the secondary lymphoid organs to the site of damage. Efferocytosis, the engulfment of cell debris and dying cells by innate immune cells, along with lymphangiogenesis, the formation of new lymphatic vessels, are emerging as central to the cardiac healing response. In this issue of the JCI, Glinton et al. used state-of-the-art approaches to demonstrate that efferocytosis induced vascular endothelial growth factor C (VEGFC) in myeloid cells and stimulated lymphangiogenesis and cardiac repair. These findings provide impactful mechanistic information that can be leveraged to therapeutically target pathways in cardiac repair and ischemic heart failure.
    MeSH term(s) Heart ; Lymphangiogenesis/physiology ; Macrophages/metabolism ; Phagocytosis ; Vascular Endothelial Growth Factor C/genetics ; Vascular Endothelial Growth Factor C/metabolism
    Chemical Substances Vascular Endothelial Growth Factor C
    Language English
    Publishing date 2022-04-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI158703
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article: Update on the Role of the Endothelial Glycocalyx in Angiogenesis and Vascular Inflammation.

    Hu, Zhengping / Cano, Issahy / D'Amore, Patricia A

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 734276

    Abstract: The endothelial glycocalyx is a negatively charged, carbohydrate-rich structure that arises from the luminal surface of the vascular endothelium and is comprised of proteoglycans, glycoproteins, and glycolipids. The glycocalyx, which sits at the ... ...

    Abstract The endothelial glycocalyx is a negatively charged, carbohydrate-rich structure that arises from the luminal surface of the vascular endothelium and is comprised of proteoglycans, glycoproteins, and glycolipids. The glycocalyx, which sits at the interface between the endothelium and the blood, is involved in a wide array of physiological and pathophysiological processes, including as a mechanotransducer and as a regulator of inflammation. Most recently, components of the glycocalyx have been shown to play a key role in controlling angiogenesis. In this review, we briefly summarize the structure and function of the endothelial glycocalyx. We focus on its role and functions in vascular inflammation and angiogenesis and discuss the important unanswered questions in this field.
    Language English
    Publishing date 2021-08-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.734276
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Endomucin selectively regulates vascular endothelial growth factor receptor-2 endocytosis through its interaction with AP2.

    Cano, Issahy / Wild, Melissa / Gupta, Urvi / Chaudhary, Suman / Ng, Yin Shan Eric / Saint-Geniez, Magali / D'Amore, Patricia A / Hu, Zhengping

    Cell communication and signaling : CCS

    2024  Volume 22, Issue 1, Page(s) 225

    Abstract: The endothelial glycocalyx, located at the luminal surface of the endothelium, plays an important role in the regulation of leukocyte adhesion, vascular permeability, and vascular homeostasis. Endomucin (EMCN), a component of the endothelial glycocalyx, ... ...

    Abstract The endothelial glycocalyx, located at the luminal surface of the endothelium, plays an important role in the regulation of leukocyte adhesion, vascular permeability, and vascular homeostasis. Endomucin (EMCN), a component of the endothelial glycocalyx, is a mucin-like transmembrane glycoprotein selectively expressed by venous and capillary endothelium. We have previously shown that knockdown of EMCN impairs retinal vascular development in vivo and vascular endothelial growth factor 165 isoform (VEGF165)-induced cell migration, proliferation, and tube formation by human retinal endothelial cells in vitro and that EMCN is essential for VEGF165-stimulated clathrin-mediated endocytosis and signaling of VEGF receptor 2 (VEGFR2). Clathrin-mediated endocytosis is an essential step in receptor signaling and is of paramount importance for a number of receptors for growth factors involved in angiogenesis. In this study, we further investigated the molecular mechanism underlying EMCN's involvement in the regulation of VEGF-induced endocytosis. In addition, we examined the specificity of EMCN's role in angiogenesis-related cell surface receptor tyrosine kinase endocytosis and signaling. We identified that EMCN interacts with AP2 complex, which is essential for clathrin-mediated endocytosis. Lack of EMCN did not affect clathrin recruitment to the AP2 complex following VEGF stimulation, but it is necessary for the interaction between VEGFR2 and the AP2 complex during endocytosis. EMCN does not inhibit VEGFR1 and FGFR1 internalization or their downstream activities since EMCN interacts with VEGFR2 but not VEGFR1 or FGFR1. Additionally, EMCN also regulates VEGF121-induced VEGFR2 phosphorylation and internalization.
    MeSH term(s) Humans ; Endothelial Cells/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; Sialomucins/metabolism ; Endocytosis ; Clathrin/metabolism
    Chemical Substances Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Sialomucins ; Clathrin
    Language English
    Publishing date 2024-04-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-024-01606-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: Macrophage efferocytosis with VEGFC and lymphangiogenesis

    Patricia A. D’Amore / Pilar Alcaide

    The Journal of Clinical Investigation, Vol 132, Iss

    rescuing the broken heart

    2022  Volume 9

    Abstract: Cardiac repair following ischemic injury is indispensable for survival and requires a coordinated cellular response involving the mobilization of immune cells from the secondary lymphoid organs to the site of damage. Efferocytosis, the engulfment of cell ...

    Abstract Cardiac repair following ischemic injury is indispensable for survival and requires a coordinated cellular response involving the mobilization of immune cells from the secondary lymphoid organs to the site of damage. Efferocytosis, the engulfment of cell debris and dying cells by innate immune cells, along with lymphangiogenesis, the formation of new lymphatic vessels, are emerging as central to the cardiac healing response. In this issue of the JCI, Glinton et al. used state-of-the-art approaches to demonstrate that efferocytosis induced vascular endothelial growth factor C (VEGFC) in myeloid cells and stimulated lymphangiogenesis and cardiac repair. These findings provide impactful mechanistic information that can be leveraged to therapeutically target pathways in cardiac repair and ischemic heart failure.
    Keywords Medicine ; R
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    More links

    Kategorien

  6. Article ; Online: Not Sure if You Are an Investigative Pathologist? Yes, You Are.

    D'Amore, Patricia A / Essex, Emily H / Furie, Martha B

    The American journal of pathology

    2021  Volume 192, Issue 1, Page(s) 2–3

    Language English
    Publishing date 2021-11-09
    Publishing country United States
    Document type Editorial
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2021.11.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Author Correction: Endomucin knockdown inhibits VEGF-induced endothelial cell migration, growth, and morphogenesis by modulating VEGFR2 signaling.

    Park-Windhol, Cindy / Ng, Yin Shan / Yang, Jinling / Primo, Vincent / Saint-Geniez, Magali / D'Amore, Patricia A

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 16620

    Language English
    Publishing date 2023-10-03
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-43612-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article ; Online: Update on the Role of the Endothelial Glycocalyx in Angiogenesis and Vascular Inflammation

    Zhengping Hu / Issahy Cano / Patricia A. D’Amore

    Frontiers in Cell and Developmental Biology, Vol

    2021  Volume 9

    Abstract: The endothelial glycocalyx is a negatively charged, carbohydrate-rich structure that arises from the luminal surface of the vascular endothelium and is comprised of proteoglycans, glycoproteins, and glycolipids. The glycocalyx, which sits at the ... ...

    Abstract The endothelial glycocalyx is a negatively charged, carbohydrate-rich structure that arises from the luminal surface of the vascular endothelium and is comprised of proteoglycans, glycoproteins, and glycolipids. The glycocalyx, which sits at the interface between the endothelium and the blood, is involved in a wide array of physiological and pathophysiological processes, including as a mechanotransducer and as a regulator of inflammation. Most recently, components of the glycocalyx have been shown to play a key role in controlling angiogenesis. In this review, we briefly summarize the structure and function of the endothelial glycocalyx. We focus on its role and functions in vascular inflammation and angiogenesis and discuss the important unanswered questions in this field.
    Keywords barrier ; leukocytes ; COVID-19 ; diabetes ; endomucin ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-08-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    More links

    Kategorien

  9. Article ; Online: Editorial.

    D'Amore, Patricia A

    Microvascular research

    2010  Volume 79, Issue 3, Page(s) 161

    MeSH term(s) Animals ; Endothelial Cells/physiology ; Humans ; Neovascularization, Physiologic ; Stem Cells/physiology
    Language English
    Publishing date 2010-05
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 80307-8
    ISSN 1095-9319 ; 0026-2862
    ISSN (online) 1095-9319
    ISSN 0026-2862
    DOI 10.1016/j.mvr.2010.02.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Galectin-3 Enhances Vascular Endothelial Growth Factor-A Receptor 2 Activity in the Presence of Vascular Endothelial Growth Factor.

    Cano, Issahy / Hu, Zhengping / AbuSamra, Dina B / Saint-Geniez, Magali / Ng, Yin Shan Eric / Argüeso, Pablo / D'Amore, Patricia A

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 734346

    Abstract: Galectin-3 (Gal3) is a carbohydrate-binding protein reported to promote angiogenesis by influencing vascular endothelial growth factor-A receptor 2 (VEGFR2) signal transduction. Here we evaluated whether the ability of Gal3 to function as an angiogenic ... ...

    Abstract Galectin-3 (Gal3) is a carbohydrate-binding protein reported to promote angiogenesis by influencing vascular endothelial growth factor-A receptor 2 (VEGFR2) signal transduction. Here we evaluated whether the ability of Gal3 to function as an angiogenic factor involved vascular endothelial growth factor (VEGF). To address this possibility we used human retinal microvascular endothelial cells (HRECs) to determine whether exogenous Gal3 requires VEGF to activate VEGFR2 signaling and if Gal3 is required for VEGF to activate VEGFR2. VEGFR2 phosphorylation and HREC migration assays, following either VEGF neutralization with ranibizumab or Gal3 silencing, revealed that VEGF endogenously produced by the HRECs was essential for the effect of exogenous Gal3 on VEGFR2 activation and cell migration, and that VEGF-induced VEGFR2 activation was not dependent on Gal3 in HRECs. Gal3 depletion led to no reduction in VEGF-induced cell function. Since Gal3 has been suggested to be a potential therapeutic target for VEGFR2-mediated angiogenesis, it is crucial to define the possible Gal3-mediated VEGFR2 signal transduction mechanism to aid the development of efficacious therapeutic strategies.
    Language English
    Publishing date 2021-09-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.734346
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top