Articles tagués Angiogenesis

Doxycycline Suppresses Cerebral MMP-9 and Angiogenesis Induced by Focal Hyperstimulation of VEGF in a Mouse Model

Doxycycline Suppresses Cerebral Matrix Metalloproteinase-9 and Angiogenesis Induced by Focal Hyperstimulation of Vascular Endothelial Growth Factor in a Mouse Model

Chanhung Z. Lee, MD, PhD; Bin Xu, MD; Tomoki Hashimoto, MD; Charles E. McCulloch, PhD; Guo-Yuan Yang, MD, PhD William L. Young, MD

Stroke. 2004;35:1715-1719 doi: 10.1161/01.STR.0000129334.05181.b6

Lire la suite »

Publicités

,

Poster un commentaire

Overexpression of delta-like 4 induces arterialization and attenuates vessel formation in developing mouse embryos

Overexpression of delta-like 4 induces arterialization and attenuates vessel formation in developing mouse embryos

Alexandre Trindade, S. Ram Kumar, Jeffrey S. Scehnet, Luis Lopes-da-Costa, Jorg Becker, Weidong Jiang, Ren Liu, Parkash S. Gill, and Antonio Duarte

Blood. 2008;112:1720-1729

Lire la suite »

, , ,

Poster un commentaire

In Vitro Differentiation of Mouse Embryonic Stem Cells Into Primitive Blood Vessels

In Vitro Differentiation of Mouse Embryonic Stem Cells Into Primitive Blood Vessels

Svetlana N. Rylova, Paramjeet K. Randhawa, and Victoria L. Bautch

Methods in Enzymology, Volume 443 DOI: 10.1016/S0076-6879(08)02006-5

Mouse embryonic stem (ES) cells, derived from the inner cell mass of blastocyst stage embryos, undergo programmed differentiation in vitro to form a primitive vasculature. This programmed differentiation proceeds through similar processes of vasculogenesis and angiogenesis found during early vascular development in vivo. Partially differentiated ES cell clumps or embryoid bodies (EBs) first form blood islands that are subsequently transformed into a network of primitive blood vessels that contain lumens. Therefore, vascular differentiation of ES cells is an ideal model to study and manipulate early vascular development. Here we provide protocols for the routine maintenance of mouse ES cells and in vitro differentiation. We also include protocols for establishing transgenic ES cell lines and visualization of blood vessels by use of endothelial specific molecular markers.

Lire la suite »

, , ,

Poster un commentaire

Three-Dimensional Analysis of Vascular Development in the Mouse Embryo

Walls JR, Coultas L, Rossant J, Henkelman RM (2008) Three-Dimensional Analysis of Vascular Development in the Mouse Embryo. PLoS ONE 3(8): e2853. doi:10.1371/journal.pone.0002853

journal.pone.0002853.g009.png

Lire la suite »

, , , ,

Poster un commentaire

Endothelial Cell Migration During Angiogenesis

Endothelial Cell Migration During Angiogenesis

Laurent Lamalice, Fabrice Le Boeuf, Jacques Huot

Circulation Research. 2007;100:782-794 doi: 10.1161/01.RES.0000259593.07661.1e

Endothelial cell migration is essential to angiogenesis. This motile process is directionally regulated by chemotactic, haptotactic, and mechanotactic stimuli and further involves degradation of the extracellular matrix to enable progression of the migrating cells. It requires the activation of several signaling pathways that converge on cytoskeletal remodeling. Then, it follows a series of events in which the endothelial cells extend, contract, and throw their rear toward the front and progress forward. The aim of this review is to give an integrative view of the signaling mechanisms that govern endothelial cell migration in the context of angiogenesis.

Lire la suite »

, , , , , , , , ,

Poster un commentaire

Role of oxygen and vascular development in epithelial branching morphogenesis of the developing mouse lung

Role of oxygen and vascular development in epithelial branching morphogenesis of the developing mouse lung

Am J Physiol Lung Cell Mol Physiol doi:10.1152/ajplung.00185.2004 288:167-178, 2005.

Minke van Tuyl, Jason Liu, Jinxia Wang, Maciek Kuliszewski, Dick Tibboel and Martin Post


zh50010520531001.gif

Fig. 1. Low oxygen enhances epithelial branching morphogenesis in vitro. C101-LacZ expression in embryonic day (E) 11.5 lung explants after 48 (A and B) and 96 (C and D) h in culture. Explants cultured at 3% oxygen (B and D) showed more complex branching compared with explants cultured at 20% oxygen (A and C). *Shows location of the trachea; arrowheads show the main bronchi, and the arrows show increased distal branch tips. Blue color is X-galactosidase (X-gal) staining in airway epithelial cells. Bars, 100 µm.


Lire la suite »

, , , , , ,

2 Commentaires

Determination of hypoxic region by hypoxia marker in developing mouse embryos in vivo: A possible signal for vessel development

Determination of hypoxic region by hypoxia marker in developing mouse embryos in vivo: A possible signal for vessel development

You Mie Lee, Chul-Ho Jeong, Sun-Young Koo, Myung Jin Son, Hyun Seok Song, Soo-Kyung Bae, James A. Raleigh, Hae-Young Chung, Mi-Ae Yoo, Kyu-Won Kim

Developmental Dynamics Volume 220 Issue 2, Pages 175 – 186, 2001

Lire la suite »

, , , , , ,

Poster un commentaire

VEGF and vascular changes in chronic neuroinflammation

VEGF and vascular changes in chronic neuroinflammation

S.L. Kirk, S.J. Karlik

Journal of Autoimmunity 21 (2003) 353–363

A vascular component has long been associated with the pathological changes in multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE). Despite the codependence of angiogenesis and many chronic inflammatory disorders, only circumstantial evidence is available to support the existence of angiogenesis in MS or EAE. To determine if angiogenesis occurs in conjunction with clinical and pathological signs of CNS inflammatory disease we evaluated temporal and spatial blood vessel counts, VEGF immunoreactivity, and histopathological changes in the spinal cord of guinea pigs with chronic-progressive (CP)-EAE (day 0–90 post-immunization, n=64) and controls (n=17). The number of vessels per section increased in infiltrated and demyelinated lesions by day 15 post-immunization and remained significantly higher than controls throughout the course of the disease. The number of vessels correlated with both clinical and pathological scores for inflammation, infiltration and demyelination. Vascular endothelial growth factor (VEGF) expression increased during acute disease peaking at day 26, which was the transition from the acute-inflammatory to chronic-demyelinating phase, before gradually returning to baseline levels. These observations implicate angiogenesis as a component of chronic neuroinflammation and demyelination and may suggest alternative therapeutic strategies for multiple sclerosis.

, , , , , ,

Poster un commentaire

Vascular Endothelial Growth Factor Up-regulates ICAM-1 Expression

Vascular Endothelial Growth Factor Up-regulates ICAM-1 Expression via the Phosphatidylinositol 3 OH-kinase/AKT/Nitric Oxide Pathway and Modulates Migration of Brain Microvascular Endothelial Cells

Zivotije Radisavljevic, Hava Avraham, and Shalom Avraham

THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 275, No. 27, Issue of July 7, pp. 20770 –20774, 2000

Endothelium of the cerebral blood microvessels, which constitutes the major component of the blood-brain barrier, controls leukocyte and metastatic cancer cell adhesion and trafficking into the brain parenchyma. In this study, using rat primary brain microvascular endothelial cells (BMEC), we demonstrate that the vascular endothelial growth factor (VEGF), a potent promoter of angiogenesis, up-regulates the expression of the intracellular adhesion molecule-1 (ICAM-1) through a novel pathway that includes phosphatidylinositol 3 OH-kinase (PI3K), AKT, and nitric oxide (NO), resulting in the migration of BMEC. Upon VEGF treatment, AKT is phosphorylated in a PI3K-dependent manner. AKT activation leads to NO production and release and activation-deficient AKT attenuates NO production stimulated by VEGF. Transfection of the constitutive myr-AKT construct significantly increased basal NO release in BMEC. In these cells, VEGF and the endothelium-derived NO synergistically up-regulated the expression of ICAM-1, which was mediated by the PI3K pathway. This activity was blocked by the PI3K-specific inhibitor, wortmannin. Furthermore, VEGF and NO significantly increased BMEC migration, which was mediated by the up-regulation of ICAM-1 expression and was dependent on the integrity of the PI3K/AKT/NO pathway. This effect was abolished by wortmannin, by the specific ICAM-1 antibody, by the specific inhibitor of NO synthase, NG-L-monomethyl-arginine (L-NMMA) or by a combination of wortmannin, ICAM-1 antibody, and L-NMMA. These findings demonstrate that the angiogenic factor VEGF up-regulates ICAM-1 expression and signals to ICAM-1 as an effector molecule through the PI3K/AKT/NO pathway, which leads to brain microvessel endothelial cell migration. These observations may contribute to a better understanding of BMEC angiogenesis and the physiological as well as pathophysiological function of the blood-brain barrier, whose integrity is crucial for normal brain function.

, , , , , , , ,

Poster un commentaire

Vascular endothelial growth factor (VEGF) modulates vascular permeability and inflammation in rat brain.

Vascular endothelial growth factor (VEGF) modulates vascular permeability and inflammation in rat brain.

Proescholdt MA, Heiss JD, Walbridge S, Mühlhauser J, Capogrossi MC, Oldfield EH, Merrill MJ.

J Neuropathol Exp Neurol. 1999 Jun;58(6):613-27

Vascular endothelial growth factor (VEGF) is an angiogenic growth factor that also induces vascular permeability and macrophage migration. VEGF expression is weak in normal adult brain, but is strongly upregulated in glioma cells and reactive astrocytes, suggesting that chronic overexpression of VEGF in the brain contributes to blood-brain barrier (BBB) breakdown. We examined the effects of chronic VEGF overexposure on the integrity of the BBB using the following approaches: 1) continuous intracerebral infusion of VEGF via miniosmotic pump; and 2) intracerebral injection of an adenoviral vector encoding the VEGF165 gene (AdCMV.VEGF). After 6 days both treatments produced approximately 10-fold breakdown of the BBB (as measured by transport of 14C-aminoisobutyric acid (AIB) from blood into brain) compared with the respective controls (albumin infusion or AdCMV.beta gal virus). BBB disruption in AdCMV.VEGF-treated brains was accompanied by a severe inflammatory response not observed in brains receiving AdCMV.beta gal or VEGF protein infusion, indicating that neither VEGF nor viral particles alone were responsible for the inflammatory response. However, injection of AdCMV.beta gal followed by VEGF infusion to the same site also elicited inflammation. Chronic overexposure of normal brain to VEGF also increased intercellular adhesion molecule-1 (ICAM-1) and major histocompatibility complex (MHC) class I and II expression. Although VEGF itself is not inflammatory, VEGF may modulate immune responses in the central nervous system (CNS) by opening the BBB, altering the immunoprivileged status of the brain, and allowing contact between normally sequestered CNS antigens and blood-borne immune mediators.

, , ,

Poster un commentaire