Assignment of Vascular Endothelial Growth Factor (VEGF) and Placenta Growth Factor (PlGF) Genes to Human Chromosome 6p12–p21 and 14q24–q31 Regions, Respectively

• Published in: Genomics (San Diego, Calif.) Calif.), 1996-02, Vol.32 (1), p.168-169
• Main Authors: Mattei, Marie-Geneviève, Borg, Jean-Paul, Rosnet, Olivier, Marmé, Dieter, Birnbaum, Daniel
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Chromosome Banding; Chromosome Mapping; Chromosomes, Human, Pair 14 - genetics; Chromosomes, Human, Pair 6 - genetics; Classical genetics, quantitative genetics, hybrids; Endothelial Growth Factors - genetics; Female; Fundamental and applied biological sciences. Psychology; Genetics of eukaryotes. Biological and molecular evolution; Growth Substances - genetics; Human; Humans; In Situ Hybridization; Lymphokines - genetics; Placenta Growth Factor; Placentation; Pregnancy; Pregnancy Proteins - genetics; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors
• ISSN: 0888-7543; 1089-8646
• DOI: 10.1006/geno.1996.0098

Angiogenesis is a crucial process during development, certain periods of adult life, and tumorigenesis and is tightly regulated by a network of growth factors and growth factor receptors. Vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) constitute a family of regulatory peptides able to control blood vessel formation and permeability by interacting with two endothelial tyrosine kinase receptors, FLT1 and KDR/FLK1, encoded by genes located, in humans, on chromosomes 13 and 4, respectively. A third member of this family could be the ligand of the related FLT4 receptor, involved in lymphatic vessel development. The genes encoding these major angiogenic factors have not been precisely localized in the human genome, although preliminary mapping has located PlGF on chromosome 14. It is of interest to determine the localization of these genes, for it may help in identifying the gene for a spontaneous mutation and associated disease. Radioactive chromosomal in situ hybridization was used to map the VEGF and PlGF genes in the human genome. The probe for human VEGF was a plasmid containing a 0.6-kb cDNA subcloned in Bluescript vector and coding for the 165-amino-acids-long form of VEGF. The probe for PlGF was a plasmid containing a 0.55-kb cDNA subcloned in Bluescript vector and coding for the 149-amino-acids-long form of PlGF. In situ hybridizations were performed according to published procedures. Briefly, experiments were carried out on chromosome preparations obtained from phytohemagglutinin-stimulated human lymphocytes cultured for 72 h. Plasmids were tritium-labeled by nick-translation to respective specific activities of 2 x 10 super(8) and 1 x 10 super(8) d.p.m. mu g super(-1) and hybridized to metaphase spreads at a final concentration of 100 ng.ml super(-1). After coating with nuclear track emulsion, the slides were exposed for 20 days. R-banding was performed by the fluorochrome-photolysis-Giemsa method (band level, 800), and metaphases were rephotographed before analysis.