The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Lena Claessonwelsh - One of the best experts on this subject based on the ideXlab platform.
-
building blood vessels stem cell models in vascular biology
Journal of Cell Biology, 2007Co-Authors: Lars Jakobsson, Johan Kreuger, Lena ClaessonwelshAbstract:Spheroids of differentiating embryonic stem cells, denoted embryoid bodies, constitute a high-quality model for vascular development, particularly well suited for loss-of-function analysis of genes required for early embryogenesis. This review examines Vasculogenesis and angiogenesis in murine embryoid bodies and discusses the promise of stem cell–based models for the study of human vascular development.
-
signal transduction by vegf receptors in regulation of angiogenesis and lymphangiogenesis
Experimental Cell Research, 2006Co-Authors: Masabumi Shibuya, Lena ClaessonwelshAbstract:The VEGF/VPF (vascular endothelial growth factor/vascular permeability factor) ligands and receptors are crucial regulators of Vasculogenesis, angiogenesis, lymphangiogenesis and vascular permeability in vertebrates. VEGF-A, the prototype VEGF ligand, binds and activates two tyrosine kinase receptors: VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). VEGFR1, which occurs in transmembrane and soluble forms, negatively regulates Vasculogenesis and angiogenesis during early embryogenesis, but it also acts as a positive regulator of angiogenesis and inflammatory responses, playing a role in several human diseases such as rheumatoid arthritis and cancer. The soluble VEGFR1 is overexpressed in placenta in preeclampsia patients. VEGFR2 has critical functions in physiological and pathological angiogenesis through distinct signal transduction pathways regulating proliferation and migration of endothelial cells. VEGFR3, a receptor for the lymphatic growth factors VEGF-C and VEGF-D, but not for VEGF-A, regulates vascular and lymphatic endothelial cell function during embryogenesis. Loss-of-function variants of VEGFR3 have been identified in lymphedema. Formation of tumor lymphatics may be stimulated by tumor-produced VEGF-C, allowing increased spread of tumor metastases through the lymphatics. Mapping the signaling system of these important receptors may provide the knowledge necessary to suppress specific signaling pathways in major human diseases.
Werner Risau - One of the best experts on this subject based on the ideXlab platform.
-
vascular endothelial growth factor vegf and vegf receptor 2 flk 1 are expressed during Vasculogenesis and vascular differentiation in the quail embryo
Developmental Biology, 1995Co-Authors: Ingo Flamme, Georg Breier, Werner RisauAbstract:Abstract Vasculogenesis, the de novo formation of embryonic blood vessels from their angioblastic precursors in situ, is supposed to be under the control of polypeptide growth factors and their receptors. The receptor tyrosine kinase flk-1 and its high-affinity ligand vascular endothelial growth factor (VEGF) represent an endothelial specific signal transduction system expressed during embryonic vascular growth in the mouse. We have cloned the quail homologs of VEGF and flk-1 using PCR and have investigated their expression pattern in vivo. As shown by Northern analysis and reverse transcription PCR, VEGF and flk-1 mRNA (3.9 and 5.8 kb, respectively) were already present in the unincubated blastodisc at low levels and were largely upregulated during gastrulation at Embryonic Day 1. As detected by in situ hybridization, flk-1 mRNA was initially present in the entire mesoderm of Day 1 embryos but from Day 2 on was restricted to endothelial cells. At Day 2 VEGF was ubiquitously expressed in the embryo proper and was mainly restricted to the vascularized part (area vasculosa) in the yolk sac. Later on VEGF expression was detected in all organs. In the kidney VEGF mRNA was mainly localized to the glomeruli. This pattern of expression is consistent with the pattern found during mouse embryogenesis. We have recently established an in vitro model of Vasculogenesis in which hemangioblastic precursors are induced in cell cultures from the unincubated quail blastodisc by basic fibroblast growth factor (bFGF) and give rise to blood vessels in vitro. Taking advantage of this in vitro model we examined whether FGF and VEGF act in concert during Vasculogenesis. We found that the flk-1 receptor mRNA is dramatically upregulated within 24 hr upon the addition of FGF to quail blastodisc cell cultures. This inducibility in response to FGF is confined to the first 24 hr of culture. The early expression of the flk-1 mRNA may characterize the differentiation of hemangioblastic precursors from pluripotent epiblast cells which in vivo is initiated during gastrulation. Thus, the time course and the pattern of expression during embryogenesis in different species suggest a major role for the VEGF/flk-1 signal transduction system in Vasculogenesis and angiogenesis.
-
induction of Vasculogenesis and hematopoiesis in vitro
Development, 1992Co-Authors: Ingo Flamme, Werner RisauAbstract:Despite a large number of investigations of embryonic vascular development, in particular in avian embryos, the conditions under which the endothelial and hematopoietic cell lineages emerge remain unknown. As we demonstrate here, both endothelial and hematopoietic cells can be induced by treatment of dissociated quail epiblast with fibroblast growth factors in vitro. These cells aggregate in characteristic blood islands. In long-term culture, the induced endothelial cells gave rise to vascular structures in vitro, i.e. Vasculogenesis. No induction was observed in the absence of fibroblast growth factors, and other growth factors like TGF-beta, TGF-alpha and EGF were not capable of inducing blood island formation. Thus, the dissociated quail epiblast provides a remarkably simple test system to investigate cell lineage diversification in higher vertebrates.
Ingo Flamme - One of the best experts on this subject based on the ideXlab platform.
-
vascular endothelial growth factor vegf and vegf receptor 2 flk 1 are expressed during Vasculogenesis and vascular differentiation in the quail embryo
Developmental Biology, 1995Co-Authors: Ingo Flamme, Georg Breier, Werner RisauAbstract:Abstract Vasculogenesis, the de novo formation of embryonic blood vessels from their angioblastic precursors in situ, is supposed to be under the control of polypeptide growth factors and their receptors. The receptor tyrosine kinase flk-1 and its high-affinity ligand vascular endothelial growth factor (VEGF) represent an endothelial specific signal transduction system expressed during embryonic vascular growth in the mouse. We have cloned the quail homologs of VEGF and flk-1 using PCR and have investigated their expression pattern in vivo. As shown by Northern analysis and reverse transcription PCR, VEGF and flk-1 mRNA (3.9 and 5.8 kb, respectively) were already present in the unincubated blastodisc at low levels and were largely upregulated during gastrulation at Embryonic Day 1. As detected by in situ hybridization, flk-1 mRNA was initially present in the entire mesoderm of Day 1 embryos but from Day 2 on was restricted to endothelial cells. At Day 2 VEGF was ubiquitously expressed in the embryo proper and was mainly restricted to the vascularized part (area vasculosa) in the yolk sac. Later on VEGF expression was detected in all organs. In the kidney VEGF mRNA was mainly localized to the glomeruli. This pattern of expression is consistent with the pattern found during mouse embryogenesis. We have recently established an in vitro model of Vasculogenesis in which hemangioblastic precursors are induced in cell cultures from the unincubated quail blastodisc by basic fibroblast growth factor (bFGF) and give rise to blood vessels in vitro. Taking advantage of this in vitro model we examined whether FGF and VEGF act in concert during Vasculogenesis. We found that the flk-1 receptor mRNA is dramatically upregulated within 24 hr upon the addition of FGF to quail blastodisc cell cultures. This inducibility in response to FGF is confined to the first 24 hr of culture. The early expression of the flk-1 mRNA may characterize the differentiation of hemangioblastic precursors from pluripotent epiblast cells which in vivo is initiated during gastrulation. Thus, the time course and the pattern of expression during embryogenesis in different species suggest a major role for the VEGF/flk-1 signal transduction system in Vasculogenesis and angiogenesis.
-
induction of Vasculogenesis and hematopoiesis in vitro
Development, 1992Co-Authors: Ingo Flamme, Werner RisauAbstract:Despite a large number of investigations of embryonic vascular development, in particular in avian embryos, the conditions under which the endothelial and hematopoietic cell lineages emerge remain unknown. As we demonstrate here, both endothelial and hematopoietic cells can be induced by treatment of dissociated quail epiblast with fibroblast growth factors in vitro. These cells aggregate in characteristic blood islands. In long-term culture, the induced endothelial cells gave rise to vascular structures in vitro, i.e. Vasculogenesis. No induction was observed in the absence of fibroblast growth factors, and other growth factors like TGF-beta, TGF-alpha and EGF were not capable of inducing blood island formation. Thus, the dissociated quail epiblast provides a remarkably simple test system to investigate cell lineage diversification in higher vertebrates.
Patricia A Damore - One of the best experts on this subject based on the ideXlab platform.
-
Vasculogenesis and angiogenesis
Cellular and Molecular Pathobiology of Cardiovascular Disease, 2014Co-Authors: Joseph F Arboledavelasquez, Patricia A DamoreAbstract:Defining angiogenesis as an organizing principle in biology and medicine indicates that there are fundamental connections between developmental and pathological phenomena that on the surface appear to be unrelated. In this chapter we discuss our current knowledge of different clinical conditions that appear to have little in common but in fact are fundamentally explained by abnormal angiogenesis that occurs as a result of congenital or postnatal aberration and/or in response to injury.
-
signal transduction in Vasculogenesis and developmental angiogenesis
The International Journal of Developmental Biology, 2011Co-Authors: Sunita Patelhett, Patricia A DamoreAbstract:The vasculature is a highly specialized organ that functions in a number of key physiological tasks including the transport of oxygen and nutrients to tissues. Formation of the vascular system is an essential and rate-limiting step in development and occurs primarily through two main mechanisms, Vasculogenesis and angiogenesis. Both Vasculogenesis, the de novo formation of vessels, and angiogenesis, the growth of new vessels from pre-existing vessels by sprouting, are complex processes that are mediated by the precise coordination of multiple cell types to form and remodel the vascular system. A host of signaling molecules and their interaction with specific receptors are central to activating and modulating vessel formation. This review article summarizes the current state of research involving signaling molecules that have been demonstrated to function in the regulation of Vasculogenesis and angiogenesis, as well as molecules known to play a role in vessel maturation, hypoxia-driven angiogenesis and arterial-venous specification.
Satoshi Murasawa - One of the best experts on this subject based on the ideXlab platform.
-
dose dependent contribution of cd34 positive cell transplantation to concurrent Vasculogenesis and cardiomyogenesis for functional regenerative recovery after myocardial infarction
Circulation, 2006Co-Authors: Hiroto Iwasaki, Atsuhiko Kawamoto, Masakazu Ishikawa, Akira Oyamada, Shuko Nakamori, Hiromi Nishimura, Kazuyo Sadamoto, Miki Horii, Tomoyuki Matsumoto, Satoshi MurasawaAbstract:Background— Multilineage developmental capacity of the CD34+ cells, especially into cardiomyocytes and smooth muscle cells (SMCs), is still controversial. In the present study we performed a series of experiments to prove our hypothesis that Vasculogenesis and cardiomyogenesis after myocardial infarction (MI) may be dose-dependently enhanced after CD34+ cell transplantation. Methods and Results— Peripheral blood CD34+ cells were isolated from total mononuclear cells of patients with limb ischemia by apheresis after 5-day administration of granulocyte colony-stimulating factor. PBS and 1×103 (low), 1×105 (mid), or 5×105 (high) CD34+ cells were intramyocardially transplanted after ligation of the left anterior descending coronary artery of nude rats. Functional assessments with the use of echocardiography and a microtip conductance catheter at day 28 revealed dose-dependent preservation of left ventricular function by CD34+ cell transplantation. Necropsy examination disclosed dose-dependent augmentation of capillary density and dose-dependent inhibition of left ventricular fibrosis. Immunohistochemistry for human-specific brain natriuretic peptide demonstrated that human cardiomyocytes were dose-dependently observed in ischemic myocardium at day 28 (high, 2480±149; mid, 1860±141; low, 423±9; PBS, 0±0/mm2; P <0.05 for high versus mid and mid versus low). Immunostaining for smooth muscle actin and human leukocyte antigen or Ulex europaeus lectin type 1 also revealed dose-dependent Vasculogenesis by endothelial cell and SMC development after CD34+ cell transplantation. Reverse transcriptase–polymerase chain reaction indicated that human-specific gene expression of cardiomyocyte (brain natriuretic peptide, cardiac troponin-I, myosin heavy chain, and Nkx 2.5), SMC (smooth muscle actin and sm22α), and endothelial cell (CD31 and KDR) markers were dose-dependently augmented in MI tissue. Conclusions— Human CD34+ cell transplantation may have significant and dose-dependent potential for Vasculogenesis and cardiomyogenesis with functional recovery from MI. Received February 8, 2005; revision received August 2, 2005; accepted September 13, 2005.
-
endothelial progenitor cells for Vasculogenesis
Physiology, 2005Co-Authors: Satoshi Murasawa, Takayuki AsaharaAbstract:Postnatal Vasculogenesis is considered to be involved in neovascularization of adult tissues, because bone marrow-derived endothelial progenitor cells (EPCs) were isolated from circulating mononuclear cells in peripheral blood and were shown to incorporate into sites of physiological and pathological neovascularization and to differentiate into mature endothelial cells. EPCs might have an attractive potential therapeutic application for cardiovascular ischemic diseases as a novel cell-based strategy mainly via a Vasculogenesis mechanism.
-
stromal cell derived factor 1 effects on ex vivo expanded endothelial progenitor cell recruitment for ischemic neovascularization
Circulation, 2003Co-Authors: Junichi Yamaguchi, Kengo Fukushima Kusano, Osamu Masuo, Atsuhiko Kawamoto, Marcy Silver, Satoshi Murasawa, Marta Boschmarce, Haruchika Masuda, Douglas W Losordo, Jeffrey M IsnerAbstract:Background— Stromal cell–derived factor-1 (SDF-1) is a chemokine considered to play an important role in the trafficking of hematopoietic stem cells. Given the close relationship between hematopoietic stem cells and endothelial progenitor cells (EPCs), we investigated the effect of SDF-1 on EPC-mediated Vasculogenesis. Methods and Results— Flow cytometric analysis demonstrated expression of CXCR4, the receptor of SDF-1, by 66±3% of EPCs after 7 days in culture. In vitro modified Boyden chamber assay showed a dose-dependent EPC migration toward SDF-1 (control versus 10 ng/mL SDF-1 versus 100 ng/mL SDF-1, 24±2 versus 71±3 versus 140±6 cells/mm2; P<0.0001). SDF-1 attenuated EPC apoptosis (control versus SDF-1, 27±1 versus 7±1%; P<0.0001). To investigate the effect of SDF-1 in vivo, we locally injected SDF-1 into athymic ischemic hindlimb muscle of nude mice combined with human EPC transplantation to determine whether SDF-1 augmented EPC-induced Vasculogenesis. Fluorescence microscopic examination disclosed i...