Person: Ng, Yin-Shan
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Yin-Shan
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Ng, Yin-Shan
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Publication Endomucin inhibits VEGF-induced endothelial cell migration, growth, and morphogenesis by modulating VEGFR2 signaling(Springer Science and Business Media LLC, 2017-12) Park-Windhol, Cindy; Ng, Yin-Shan; Yang, Jinling; Primo, Vincent; Saint-Geniez, Magali; D’Amore, Patricia A.Publication VEGF164-mediated Inflammation Is Required for Pathological, but Not Physiological, Ischemia-induced Retinal Neovascularization(Rockefeller University Press, 2003) Ishida, Susumu; Usui, Tomohiko; Yamashiro, Kenji; Kaji, Yuichi; Amano, Shiro; Ogura, Yuichiro; Hida, Tetsuo; Oguchi, Yoshihisa; Ambati, Jayakrishna; Miller, Joan; Gragoudas, Evangelos; Ng, Yin-Shan; D'Amore, Patricia; Shima, David T.; Adamis, AnthonyHypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls. In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte–mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined.Publication Skeletal defects in VEGF120/120 mice reveal multiple roles for VEGF in skeletogenesis(The Company of Biologists, 2002) Zelzer, Elazar; McLean, William; Ng, Yin-Shan; Fukai, Naomi; Reginato, Anthony; Lovejoy, Stephanie; D'Amore, Patricia; Olsen, BjornAngiogenesis is an essential component of skeletal development and VEGF signaling plays an important if not pivotal role in this process. Previous attempts to examine the roles of VEGF in vivo have been largely unsuccessful because deletion of even one VEGF allele leads to embryonic lethality before skeletal development is initiated. The availability of mice expressing only the VEGF120 isoform (which do survive to term) has offered an opportunity to explore the function of VEGF during embryonic skeletal development. Our study of these mice provides new in vivo evidence for multiple important roles of VEGF in both endochondral and intramembranous bone formation, as well as some insights into isoform-specific functions. There are two key differences in vascularization of developing bones between wild-type and VEGF120/120 mice. VEGF120/120 mice have not only a delayed recruitment of blood vessels into the perichondrium but also show delayed invasion of vessels into the primary ossification center, demonstrating a significant role of VEGF at both an early and late stage of cartilage vascularization. These findings are the basis for a two-step model of VEGF-controlled vascularization of the developing skeleton, a hypothesis that is supported by the new finding that VEGF is expressed robustly in the perichondrium and surrounding tissue of cartilage templates of future bones well before blood vessels appear in these regions. We also describe new in vivo evidence for a possible role of VEGF in chondrocyte maturation, and document that VEGF has a direct role in regulating osteoblastic activity based on in vivo evidence and organ culture experiments.Publication Arteriolar and venular patterning in retinas of mice selectively expressing VEGF isoforms(American Society for Clinical Investigation, 2002) Stalmans, Ingeborg; Ng, Yin-Shan; Rohan, Richard; Fruttiger, Marcus; Bouché, Ann; Yuce, Ali; Fujisawa, Hajime; Hermans, Bart; Shani, Moshe; Jansen, Sandra; Hicklin, Dan; Anderson, David J.; Gardiner, Tom; Hammes, Hans-Peter; Moons, Lieve; Dewerchin, Mieke; Collen, Désiré; Carmeliet, Peter; D'Amore, PatriciaThe murine VEGF gene is alternatively transcribed to yield the VEGF120, VEGF164, and VEGF188 isoforms, which differ in their potential to bind to heparan sulfate and neuropilin-1 and to stimulate endothelial growth. Here, their role in retinal vascular development was studied in mice selectively expressing single isoforms. VEGF164/164 mice were normal, healthy, and had normal retinal angiogenesis. In contrast, VEGF120/120 mice exhibited severe defects in vascular outgrowth and patterning, whereas VEGF188/188 mice displayed normal venular outgrowth but impaired arterial development. It is noteworthy that neuropilin-1, a receptor for VEGF164, was predominantly expressed in retinal arterioles. These findings reveal distinct roles of the various VEGF isoforms in vascular patterning and arterial development in the retina.Publication Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres(MyJove Corporation, 2015) Bunker, Shannon; Holeniewska, Joanna; Vijay, Sauparnika; Dahlmann-Noor, Annegret; Khaw, Peng; Ng, Yin-Shan; Shima, David; Foxton, RichardProgress in understanding the pathophysiology, and providing novel treatments for glaucoma is dependent on good animal models of the disease. We present here a protocol for elevating intraocular pressure (IOP) in the rat, by injecting magnetic microspheres into the anterior chamber of the eye. The use of magnetic particles allows the user to manipulate the beads into the iridocorneal angle, thus providing a very effective blockade of fluid outflow from the trabecular meshwork. This leads to long-lasting IOP rises, and eventually neuronal death in the ganglion cell layer (GCL) as well as optic nerve pathology, as seen in patients with the disease. This method is simple to perform, as it does not require machinery, specialist surgical skills, or many hours of practice to perfect. Furthermore, the pressure elevations are very robust, and reinjection of the magnetic microspheres is not usually required unlike in some other models using plastic beads. Additionally, we believe this method is suitable for adaptation for the mouse eye.