Abstract

We report here the cloning and characterization of human and mouse genes for vascular endothelial growth factor C (VEGF-C), a newly isolated member of the vascular endothelial growth factor/platelet-derived growth factor (VEGF/PDGF) family. Both VEGF-C genes comprise over 40 kilobase pairs of genomic DNA and consist of seven exons, all containing coding sequences. The VEGF homology domain of VEGF-C is encoded by exons 3 and 4. Exons 5 and 7 encode cysteine-rich motifs of the type C6C10CRC, and exon 6 encodes additional C10CXCXC motifs typical of a silk protein. A putative alternatively spliced rare RNA form lacking exon 4 was identified in human fibrosarcoma cells, and a major transcription start site was located in the human VEGF-C gene 523 base pairs upstream of the translation initiation codon. The upstream promoter sequences contain conserved putative binding sites for Sp-1, AP-2, and NF-kappaB transcription factors but no TATA box, and they show promoter activity when transfected into cells. The VEGF-C gene structure is thus assembled from exons encoding propeptides and distinct cysteine-rich domains in addition to the VEGF homology domain, and it shows both similarities and distinct differences in comparison with other members of the VEGF/PDGF gene family.

Highlights

  • The process of growth and development of new blood vessels from preexisting ones is termed angiogenesis

  • vascular endothelial growth factor C (VEGF-C) is the fourth member of the vascular endothelial growth factor (VEGF) subfamily of PDGF-related growth factors and the largest VEGF gene described so far

  • The genomic structures of the previously described members, VEGF, VEGF-B, and placenta growth factor (PlGF) show a high degree of similarity between each other in exon-intron junctions and some similarities of alternative splicing

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Summary

Introduction

The process of growth and development of new blood vessels from preexisting ones is termed angiogenesis. VEGF is implicated in vasculogenesis or formation of blood vessels de novo by in situ differentiation from mesodermal precursor cells [7]. The human promoter was shown to contain multiple binding sites for Sp-1, AP-1, and AP-2 transcription factors and hypoxia-regulated elements [21,22,23]. This promoter is TATAless and responds to various effectors, including hypoxia, tumor necrosis factor-␣, and basic fibroblast growth factor [24]. We show that human genomic fragments containing the transcription initiation site are sufficient for basal promoter activity in transfected cells

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