References of "Moons, Lieve"
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailInvolvement of placental growth factor in Wallerian degeneration
Chaballe, Linda ULg; Close, Pierre ULg; SEMPELS, Maxime ULg et al

in Glia (2011), 59(3), 379-396

Wallerian degeneration (WD) is an inflammatory process of nerve degeneration, which occurs more rapidly in the peripheral nervous system compared with the central nervous system, resulting, respectively ... [more ▼]

Wallerian degeneration (WD) is an inflammatory process of nerve degeneration, which occurs more rapidly in the peripheral nervous system compared with the central nervous system, resulting, respectively in successful and aborted axon regeneration. In the peripheral nervous system, Schwann cells (SCs) and macrophages, under the control of a network of cytokines and chemokines, represent the main cell types involved in this process. Within this network, the role of placental growth factor (PlGF) remains totally unknown. However, properties like monocyte activation/attraction, ability to increase expression of pro-inflammatory molecules, as well as neuroprotective effects, make it a candidate likely implicated in this process. Also, nothing is described about the expression and localization of this molecule in the peripheral nervous system. To address these original questions, we decided to study PlGF expression under physiological and degenerative conditions and to explore its role in WD, using a model of sciatic nerve transection in wild-type and Pgf(-/-) mice. Our data show dynamic changes of PlGF expression, from periaxonal in normal nerve to SCs 24h postinjury, in parallel with a p65/NF-κB recruitment on Pgf promoter. After injury, SC proliferation is reduced by 30% in absence of PlGF. Macrophage invasion is significantly delayed in Pgf(-/-) mice compared with wild-type mice, which results in worse functional recovery. MCP-1 and proMMP-9 exhibit a 3-fold reduction of their relative expressions in Pgf(-/-) injured nerves, as demonstrated by cytokine array. In conclusion, this work originally describes PlGF as a novel member of the cytokine network of WD. [less ▲]

Detailed reference viewed: 59 (21 ULg)
Full Text
See detailInvolvement of Placental growth factor in Wallerian degeneration
Chaballe, Linda ULg; Close, Pierre ULg; Sempels, Maxime ULg et al

Poster (2010, September)

Detailed reference viewed: 32 (11 ULg)
Full Text
Peer Reviewed
See detailModeling Lymphangiogenesis in a three-dimensional culture system
Bruyere, Françoise; Melen-Lamalle, Laurence; Blacher, Silvia ULg et al

in Nature Methods (2008), 5(5), 431-437

Unraveling the molecular mechanisms of lymphangiogenesis is hampered by the lack of appropriate in vitro models of three-dimensional (3D) lymph vessel growth which can be used to exploit the potential of ... [more ▼]

Unraveling the molecular mechanisms of lymphangiogenesis is hampered by the lack of appropriate in vitro models of three-dimensional (3D) lymph vessel growth which can be used to exploit the potential of available transgenic mice. We developed a potent reproducible and quantifiable 3D-culture system of lymphatic endothelial cells, the lymphatic ring assay, bridging the gap between 2D-in vitro and in vivo models of lymphangiogenesis. Mice thoracic duct fragments are embedded in a collagen gel leading to the formation of lymphatic capillaries containing a lumen as assessed by electron microscopy and immunostaining. This assay phenocopies the different steps of lymphangiogenesis, including the spreading from a preexisting vessel, cell proliferation, migration and differentiation into capillaries. Our study provides evidence for the implication of an individual matrix metalloproteinase, MMP-2, during lymphangiogenesis. The lymphatic ring assay is a robust, quantifiable and reproducible system which offers new opportunities for rapid identification of unknown regulators of lymphangiogenesis. [less ▲]

Detailed reference viewed: 132 (25 ULg)
Full Text
Peer Reviewed
See detailDeficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.
Aragones, Julian; Schneider, Martin; Van Geyte, Katie et al

in Nature Genetics (2008), 40

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen ... [more ▼]

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia. Hypoxia tolerance is not due to HIF-dependent angiogenesis, erythropoiesis or vasodilation, but rather to reduced generation of oxidative stress, which allows Phd1-deficient myofibers to preserve mitochondrial respiration. Hypoxia tolerance relies primarily on Hif-2alpha and was not observed in heterozygous Phd2-deficient or homozygous Phd3-deficient mice. Of medical importance, conditional knockdown of Phd1 also rapidly induces hypoxia tolerance. These findings delineate a new role of Phd1 in hypoxia tolerance and offer new treatment perspectives for disorders characterized by oxidative stress. [less ▲]

Detailed reference viewed: 43 (10 ULg)
Full Text
Peer Reviewed
See detailSynergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions
Carmeliet, Peter; Moons, Lieve; Luttun, Aernout et al

in Nature Medicine (2001), 7(5), 575-583

Vascular endothelial growth factor (VEGF) stimulates angiogenesis by activating VEGF receptor-2 (VEGFR-2). The role of its homolog, placental growth factor (PlGF), remains unknown. Both VEGF and PlGF bind ... [more ▼]

Vascular endothelial growth factor (VEGF) stimulates angiogenesis by activating VEGF receptor-2 (VEGFR-2). The role of its homolog, placental growth factor (PlGF), remains unknown. Both VEGF and PlGF bind to VEGF receptor-1 (VEGFR-1), but it is unknown whether VEGFR-1, which exists as a soluble or a membrane-bound type, is an inert decoy or a signaling receptor for PlGF during angiogenesis. Here, we report that embryonic angiogenesis in mice was not affected by deficiency of PlGF (Pgf -/-). VEGF-B, another ligand of VEGFR-1, did not rescue development in Pgf -/- mice. However, loss of PlGF impaired angiogenesis, plasma extravasation and collateral growth during ischemia, inflammation, wound healing and cancer. Transplantation of wild-type bone marrow rescued the impaired angiogenesis and collateral growth in Pgf -/- mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow−derived cells. The synergism between PlGF and VEGF was specific, as PlGF deficiency impaired the response to VEGF, but not to bFGF or histamine. VEGFR-1 was activated by PlGF, given that anti-VEGFR-1 antibodies and a Src-kinase inhibitor blocked the endothelial response to PlGF or VEGF/PlGF. By upregulating PlGF and the signaling subtype of VEGFR-1, endothelial cells amplify their responsiveness to VEGF during the 'angiogenic switch' in many pathological disorders. [less ▲]

Detailed reference viewed: 387 (7 ULg)