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      Ets Motifs Are Necessary for Endothelial Cell–Specific Expression of a 723-bp Tie-2 Promoter/Enhancer in Hprt Targeted Transgenic Mice

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          Abstract

          Tie-2 is an endothelial cell-specific receptor tyrosine kinase that is involved in the remodeling of blood vessels and angiogenesis. Our goal was to characterize Tie-2 promoter function as a means of providing insight into the mechanisms of endothelial cell-specific gene regulation.

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          Uniform vascular-endothelial-cell-specific gene expression in both embryonic and adult transgenic mice.

          Thorsten Schlaeger, Takashi Sato, J Lawitts … (1997)
          TIE2 is a vascular endothelial-specific receptor tyrosine kinase essential for the regulation of vascular network formation and remodeling. Previously, we have shown that the 1.2-kb 5' flanking region of the TIE2 promoter is capable of directing beta-galactosidase reporter gene expression specifically into a subset of endothelial cells (ECs) of transgenic mouse embryos. However, transgene activity was restricted to early embryonic stages and not detectable in adult mice. Herein we describe the identification and characterization of an autonomous endothelial-specific enhancer in the first intron of the mouse TIE2 gene. Furthermore, combination of the TIE2 promoter with an intron fragment containing this enhancer allows it to target reporter gene expression specifically and uniformly to virtually all vascular ECs throughout embryogenesis and adulthood. To our knowledge, this is the first time that an in vivo expression system has been assembled by which heterologous genes can be targeted exclusively to the ECs of the entire vasculature. This should be a valuable tool to address the function of genes during physiological and pathological processes of vascular ECs in vivo. Furthermore, we were able to identify a short region critical for enhancer function in vivo that contains putative binding sites for Ets-like transcription factors. This should, therefore, allow us to determine the molecular mechanisms underlying the vascular-EC-specific expression of the TIE2 gene.
          Article 0 comments Cited 64 times – based on 0 reviews     Review now
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            [36] Eukaryotic gene transcription with purified components

            John D. Dignam, Paul Martin, Barkur S Shastry … (1983)
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              Cloning and functional analysis of the promoter for KDR/flk-1, a receptor for vascular endothelial growth factor.

              James Haber, M Perrella, Marc Patterson … (1995)
              KDR/flk-1 is one of two receptors for vascular endothelial growth factor, a potent angiogenic peptide. KDR/flk-1 is an early marker for endothelial cell progenitors, and its expression is restricted to endothelial cells in vivo. To investigate the molecular mechanisms regulating expression of KDR/flk-1, we cloned and characterized the promoter of the human KDR/flk-1 gene. The transcription start site was localized by primer extension and ribonuclease protection to a nucleotide 303 base pairs (bp) 5' of the initiation methionine codon. The 5'-flanking sequence is rich in G and C residues and contains five Sp1 elements but no TATA consensus sequence. By reporter gene transfection experiments, we found that approximately 4 kilobases of KDR/flk-1 5'-flanking sequence directed high level luciferase activity in bovine aortic endothelial cells; further deletion analysis revealed positive regulatory elements between bp -225 to -164, -95 to -77, -77 to -60, and +105 to +127. Mutation of an atypical GATA sequence between bp +105 and +127 did not affect promoter activity, suggesting that GATA elements are not essential for the high level promoter activity of this gene. Consistent with endothelial cell-restricted expression of KDR/flk-1 mRNA, we found that the 4-kilobase flanking sequence directed high level promoter activity in endothelial cells but not in other cell types. To our knowledge this is the first report characterizing the KDR/flk-1 promoter. Understanding the KDR/flk-1 promoter will allow us to investigate endothelial cell-specific gene regulation and to uncover methods for targeting gene delivery specifically to endothelial cells.
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                Author and article information

                Journal
                Title: Arteriosclerosis, Thrombosis, and Vascular Biology
                Abbreviated Title: ATVB
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 1079-5642
                ISSN (Electronic): 1524-4636
                Publication date Created: November 2003
                Publication date (Print): November 2003
                Volume: 23
                Issue: 11
                Pages: 2041-2047
                Affiliations
                [1 ]From the Research Center for Advanced Science and Technology (T.M., T.K.), University of Tokyo, Japan; Department of Molecular Medicine (T.M., W.C.A., R.D.R.), Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, Mass; and Department of Biology (J.A.K., V.E., R.D.R.), Massachusetts Institute of Technology, Cambridge, Mass.
                Article
                DOI: 10.1161/01.ATV.0000089326.63053.9A
                PubMed ID: 12893685
                SO-VID: 07f98f9a-1dfa-47bd-b9b0-a76130fbc4fc
                Copyright © © 2003
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