The Experts below are selected from a list of 286224 Experts worldwide ranked by ideXlab platform

Karen K Hirschi - One of the best experts on this subject based on the ideXlab platform.

  • retinoic acid promotes Endothelial Cell cycle early g1 state to enable human hemogenic Endothelial Cell specification
    Cell Reports, 2020
    Co-Authors: Jingyao Qiu, Sofia Nordling, Hema Vasavada, Eugene C Butcher, Karen K Hirschi
    Abstract:

    Summary Development of blood-forming (hemogenic) Endothelial Cells that give rise to hematopoietic stem and progenitor Cells (HSPCs) is critical during embryogenesis to generate the embryonic and postnatal hematopoietic system. We previously demonstrated that the specification of murine hemogenic Endothelial Cells is promoted by retinoic acid (RA) signaling and requires downstream Endothelial Cell cycle control. Whether this mechanism is conserved in human hemogenic Endothelial Cell specification is unknown. Here, we present a protocol to derive primordial Endothelial Cells from human embryonic stem Cells and promote their specification toward hemogenic Endothelial Cells. Furthermore, we demonstrate that RA treatment significantly increases human hemogenic Endothelial Cell specification. That is, RA promotes Endothelial Cell cycle arrest to enable RA-induced instructive signals to upregulate the genes needed for hematopoietic transition. These insights provide guidance for the ex vivo generation of autologous human hemogenic Endothelial Cells that are needed to produce human HSPCs for regenerative medicine applications.

  • retinoic acid promotes Endothelial Cell cycle early g1 state to enable human hemogenic Endothelial Cell specification
    2020
    Co-Authors: Jingyao Qiu, Sofia Nordling, Hema Vasavada, Eugene C Butcher, Karen K Hirschi
    Abstract:

    Development of blood-forming (hemogenic) Endothelial Cells that give rise to hematopoietic stem and progenitor Cells (HSPC) is critical during embryogenesis to generate the embryonic and postnatal hematopoietic system. We previously demonstrated that specification of murine hemogenic Endothelial Cells is promoted by retinoic acid (RA) signaling and requires downstream Endothelial Cell cycle control. Whether this mechanism is conserved in human hemogenic Endothelial Cell specification is unknown. Here, we present a novel protocol to derive Endothelial Cells, hemogenic Endothelial Cells and blood Cells from human embryonic stem Cells. Using this model, we demonstrate that RA and Cell cycle control play essential roles in human hemogenic Endothelial Cell specification. That is, RA promotes Endothelial Cell cycle arrest to enable RA-induced instructive signals to upregulate hematopoietic gene expression. These novel insights will provide guidance for the ex vivo generation of autologous human HSPC for regenerative medicine applications.

  • retinoic acid regulates Endothelial Cell proliferation during vasculogenesis
    Development, 2003
    Co-Authors: Brenda L. Bohnsack, Karen Niederreither, Karen K Hirschi
    Abstract:

    A dietary deficiency of vitamin A is associated with cardiovascular abnormalities in avian and murine systems. Retinoic acid (RA) is the active metabolite of vitamin A and whether it directly regulates mammalian blood vessel formation has not been determined and is investigated herein. We used mice rendered RA-deficient via targeted deletion of retinaldehyde dehydrogenase 2 ( Raldh2 -/- ), the enzyme required to produce active RA in the embryo. Histological examination at E8.0-8.5, prior to cardiac function and systemic blood circulation, revealed that capillary plexi formed in Raldh2 -/- yolk sacs and embryos, but were dilated, and not appropriately remodeled or patterned. Raldh2 -/- Endothelial Cells exhibited significantly increased expression of phosphohistone 3 and decreased expression of p21 and p27, suggesting that RA is required to control Endothelial Cell cycle progression during early vascular development. Uncontrolled Endothelial Cell growth, in Raldh2 -/- mutants, was associated with decreased Endothelial Cell maturation, disrupted vascular plexus remodeling and lack of later stages of vessel assembly, including mural Cell differentiation. Maternally administrated RA restored Endothelial Cell cycle control and vascular patterning. Thus, these data indicate that RA plays a crucial role in mammalian vascular development; it is required to control Endothelial Cell proliferation and vascular remodeling during vasculogenesis.

Eugene C Butcher - One of the best experts on this subject based on the ideXlab platform.

  • retinoic acid promotes Endothelial Cell cycle early g1 state to enable human hemogenic Endothelial Cell specification
    Cell Reports, 2020
    Co-Authors: Jingyao Qiu, Sofia Nordling, Hema Vasavada, Eugene C Butcher, Karen K Hirschi
    Abstract:

    Summary Development of blood-forming (hemogenic) Endothelial Cells that give rise to hematopoietic stem and progenitor Cells (HSPCs) is critical during embryogenesis to generate the embryonic and postnatal hematopoietic system. We previously demonstrated that the specification of murine hemogenic Endothelial Cells is promoted by retinoic acid (RA) signaling and requires downstream Endothelial Cell cycle control. Whether this mechanism is conserved in human hemogenic Endothelial Cell specification is unknown. Here, we present a protocol to derive primordial Endothelial Cells from human embryonic stem Cells and promote their specification toward hemogenic Endothelial Cells. Furthermore, we demonstrate that RA treatment significantly increases human hemogenic Endothelial Cell specification. That is, RA promotes Endothelial Cell cycle arrest to enable RA-induced instructive signals to upregulate the genes needed for hematopoietic transition. These insights provide guidance for the ex vivo generation of autologous human hemogenic Endothelial Cells that are needed to produce human HSPCs for regenerative medicine applications.

  • retinoic acid promotes Endothelial Cell cycle early g1 state to enable human hemogenic Endothelial Cell specification
    2020
    Co-Authors: Jingyao Qiu, Sofia Nordling, Hema Vasavada, Eugene C Butcher, Karen K Hirschi
    Abstract:

    Development of blood-forming (hemogenic) Endothelial Cells that give rise to hematopoietic stem and progenitor Cells (HSPC) is critical during embryogenesis to generate the embryonic and postnatal hematopoietic system. We previously demonstrated that specification of murine hemogenic Endothelial Cells is promoted by retinoic acid (RA) signaling and requires downstream Endothelial Cell cycle control. Whether this mechanism is conserved in human hemogenic Endothelial Cell specification is unknown. Here, we present a novel protocol to derive Endothelial Cells, hemogenic Endothelial Cells and blood Cells from human embryonic stem Cells. Using this model, we demonstrate that RA and Cell cycle control play essential roles in human hemogenic Endothelial Cell specification. That is, RA promotes Endothelial Cell cycle arrest to enable RA-induced instructive signals to upregulate hematopoietic gene expression. These novel insights will provide guidance for the ex vivo generation of autologous human HSPC for regenerative medicine applications.

Kenneth A Thomas - One of the best experts on this subject based on the ideXlab platform.

  • Specificity of vascular Endothelial Cell growth factor receptor ligand binding domains.
    Biochemical and biophysical research communications, 1994
    Co-Authors: R. L. Kendall, Guan Wang, J. Disalvo, Kenneth A Thomas
    Abstract:

    Vascular Endothelial Cell growth factor binds with high affinity to FLT and KDR, two homologous tyrosine kinase receptors expressed on vascular Endothelial Cells. Placental growth factor, a vascular Endothelial Cell growth factor homologue, also binds with high affinity to the extraCellular domains of FLT but not to the extraCellular region of KDR. Vascular Endothelial Cell growth factor binds competitively with placental growth factor to the extraCellular ligand binding domains of FLT, indicating that both ligands probably complex to overlapping or identical regions of this receptor.

  • inhibition of vascular Endothelial Cell growth factor activity by an endogenously encoded soluble receptor
    Proceedings of the National Academy of Sciences of the United States of America, 1993
    Co-Authors: Richard L Kendall, Kenneth A Thomas
    Abstract:

    Abstract Vascular Endothelial Cell growth factor, a mitogen selective for vascular Endothelial Cells in vitro that promotes angiogenesis in vivo, functions through distinct membrane-spanning tyrosine kinase receptors. The cDNA encoding a soluble truncated form of one such receptor, fms-like tyrosine kinase receptor, has been cloned from a human vascular Endothelial Cell library. The mRNA coding region distinctive to this cDNA has been confirmed to be present in vascular Endothelial Cells. Soluble fms-like tyrosine kinase receptor mRNA, generated by alternative splicing of the same pre-mRNA used to produce the full-length membrane-spanning receptor, encodes the six N-terminal immunoglobulin-like extraCellular ligand-binding domains but does not encode the last such domain, transmembrane-spanning region, and intraCellular tyrosine kinase domains. The recombinant soluble human receptor binds vascular Endothelial Cell growth factor with high affinity and inhibits its mitogenic activity for vascular Endothelial Cells; thus this soluble receptor could act as an efficient specific antagonist of vascular Endothelial Cell growth factor in vivo.

Jingyao Qiu - One of the best experts on this subject based on the ideXlab platform.

  • retinoic acid promotes Endothelial Cell cycle early g1 state to enable human hemogenic Endothelial Cell specification
    Cell Reports, 2020
    Co-Authors: Jingyao Qiu, Sofia Nordling, Hema Vasavada, Eugene C Butcher, Karen K Hirschi
    Abstract:

    Summary Development of blood-forming (hemogenic) Endothelial Cells that give rise to hematopoietic stem and progenitor Cells (HSPCs) is critical during embryogenesis to generate the embryonic and postnatal hematopoietic system. We previously demonstrated that the specification of murine hemogenic Endothelial Cells is promoted by retinoic acid (RA) signaling and requires downstream Endothelial Cell cycle control. Whether this mechanism is conserved in human hemogenic Endothelial Cell specification is unknown. Here, we present a protocol to derive primordial Endothelial Cells from human embryonic stem Cells and promote their specification toward hemogenic Endothelial Cells. Furthermore, we demonstrate that RA treatment significantly increases human hemogenic Endothelial Cell specification. That is, RA promotes Endothelial Cell cycle arrest to enable RA-induced instructive signals to upregulate the genes needed for hematopoietic transition. These insights provide guidance for the ex vivo generation of autologous human hemogenic Endothelial Cells that are needed to produce human HSPCs for regenerative medicine applications.

  • retinoic acid promotes Endothelial Cell cycle early g1 state to enable human hemogenic Endothelial Cell specification
    2020
    Co-Authors: Jingyao Qiu, Sofia Nordling, Hema Vasavada, Eugene C Butcher, Karen K Hirschi
    Abstract:

    Development of blood-forming (hemogenic) Endothelial Cells that give rise to hematopoietic stem and progenitor Cells (HSPC) is critical during embryogenesis to generate the embryonic and postnatal hematopoietic system. We previously demonstrated that specification of murine hemogenic Endothelial Cells is promoted by retinoic acid (RA) signaling and requires downstream Endothelial Cell cycle control. Whether this mechanism is conserved in human hemogenic Endothelial Cell specification is unknown. Here, we present a novel protocol to derive Endothelial Cells, hemogenic Endothelial Cells and blood Cells from human embryonic stem Cells. Using this model, we demonstrate that RA and Cell cycle control play essential roles in human hemogenic Endothelial Cell specification. That is, RA promotes Endothelial Cell cycle arrest to enable RA-induced instructive signals to upregulate hematopoietic gene expression. These novel insights will provide guidance for the ex vivo generation of autologous human HSPC for regenerative medicine applications.

Shane P. Herbert - One of the best experts on this subject based on the ideXlab platform.

  • molecular control of Endothelial Cell behaviour during blood vessel morphogenesis
    Nature Reviews Molecular Cell Biology, 2011
    Co-Authors: Shane P. Herbert, Didier Y R Stainier
    Abstract:

    The vertebrate vasculature forms an extensive branched network of blood vessels that supplies tissues with nutrients and oxygen. During vascular development, coordinated control of Endothelial Cell behaviour at the levels of Cell migration, proliferation, polarity, differentiation and Cell-Cell communication is critical for functional blood vessel morphogenesis. Recent data uncover elaborate transcriptional, post-transcriptional and post-translational mechanisms that fine-tune key signalling pathways (such as the vascular Endothelial growth factor and Notch pathways) to control Endothelial Cell behaviour during blood vessel sprouting (angiogenesis). These emerging frameworks controlling angiogenesis provide unique insights into fundamental biological processes common to other systems, such as tissue branching morphogenesis, mechanotransduction and tubulogenesis.

  • molecular control of Endothelial Cell behaviour during blood vessel morphogenesis
    Nature Reviews Molecular Cell Biology, 2011
    Co-Authors: Shane P. Herbert, Didier Y R Stainier
    Abstract:

    The coordinated control of Endothelial Cell behaviour is critical for blood vessel morphogenesis. Recent data reveal elaborate mechanisms that fine-tune key signalling pathways (such as the vascular Endothelial growth factor and Notch pathways) to control Endothelial Cell behaviour during blood vessel sprouting (angiogenesis).