NDLI: Transgenic induction of vascular endothelial growth factor-C is strongly angiogenic in mouse embryos but leads to persistent lymphatic hyperplasia in adult tissues.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lohela, Marja Heloterä, Hanna Haiko, Paula Dumont, Daniel J. Alitalo, Kari
Description	Country affiliation: Finland Author Affiliation: Lohela M ( Molecular/Cancer Biology Laboratory, Biomedicum Helsinki, University of Helsinki, Finland.)
Abstract	Vascular endothelial growth factor-C (VEGF-C) is the quintessential lymphangiogenic growth factor that is required for the development of the lymphatic system and is capable of stimulating lymphangiogenesis in adults by activating its receptor, VEGFR-3. Although VEGF-C is a major candidate molecule for the development of prolymphangiogenic therapy for defective lymphatic vessels in lymphedema, the stability of lymph vessels generated by exogenous VEGF-C administration is not currently known. We studied VEGF-C-stimulated lymphangiogenesis in inducible transgenic mouse models in which growth factor expression can be spatially and temporally controlled without side effects, such as inflammation. VEGF-C induction in adult mouse skin for 1 to 2 weeks caused robust lymphatic hyperplasia that persisted for at least 6 months. VEGF-C induced lymphangiogenesis in numerous tissues and organs when expressed in the vascular endothelium in either neonates or adult mice. Very few or no effects were observed in either blood vessels or collecting lymph vessels. Additionally, VEGF-C stimulated lymphangiogenesis in embryos after the onset of lymphatic vessel development. Strikingly, a strong angiogenic effect was observed after VEGF-C induction in vascular endothelium at any point before embryonic day 16.5. Our results indicate that blood vessels can undergo VEGF-C-induced angiogenesis even after down-regulation of VEGFR-3 in embryos; however, transient VEGF-C expression in adults can induce long-lasting lymphatic hyperplasia with no obvious side effects on the blood vasculature.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.2353/ajpath.2008.080378
Journal	The American Journal of Pathology
Issue Number	6
Volume Number	173
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2008-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, Non-u.s. Gov't Vascular Endothelial Growth Factor C Endothelial Cells Embryo, Mammalian Biological Markers Hyperplasia Cytology Vascular Endothelial Growth Factor Receptor-3 Lymphatic Vessels Genetics Physiology Lymphangiogenesis Transgenes Tyrosine Antigens, Cd31 Anatomy & Histology Mice, Transgenic Discipline Pathology Glycoproteins Metabolism Pregnancy Pathology Animals Mice Neovascularization, Physiologic
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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