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      Endothelial-Specific Cre Mouse Models : Is Your Cre CREdibile?

      Author(s): 1 , 1 , 2 , 2
      Publication date Created:
      Publication date (Print):
      Journal: Arteriosclerosis, Thrombosis, and Vascular Biology
      Publisher: Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          <p class="first" id="P1">The field of vascular biology has gained enormous insight from the use of Cre and Cre/ERT2 mouse models to temporally and spatially manipulate gene expression within the endothelium. Models are available to constitutively or inducibly modulate gene expression in all, or a specified subset of endothelial cells (ECs). However, caution should be applied to both the selection of allele and the analysis of resultant phenotype: many similarly-named Cre models have divergent activity patterns, while ectopic or inconsistent Cre or Cre/ERT2 expression can dramatically affect results. In an effort to disambiguate previous data and to provide a resource to aid appropriate experimental design, here we summarise what is known about Cre recombinase activity in the most widely used endothelial-specific Cre and Cre/ERT2 mouse models. </p>

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          Pericyte loss and microaneurysm formation in PDGF-B-deficient mice.

          P Lindahl, B R Johansson, P Levéen … (1997)
          Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.
          Article 0 comments Cited 450 times – based on 0 reviews     Review now
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            Regulation of Cre recombinase activity by mutated estrogen receptor ligand-binding domains.

            R Feil, J. Wagner, D. Metzger … (1997)
            Ligand-dependent chimeric Cre recombinases are powerful tools to induce specific DNA rearrangements in cultured cells and in mice. We report here the construction and characterization of a series of chimeric recombinases, each consisting of Cre fused to a mutated human oestrogen receptor (ER) ligand-binding domain (LBD). Two new ligand-dependent recombinases which contain either the G400V/M543A/L544A or the G400V/L539A/L540A triple mutation of the human ER LBD are efficiently induced by the synthetic ER antagonists 4-hydroxytamoxifen (OHT) and ICI 182,780 (ICI), respectively, but are insensitive to 17 beta-oestradiol (E2). Both chimeric recombinases should be useful for efficient spatio-temporally controlled site-directed somatic mutagenesis.
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              Identification and functional analysis of endothelial tip cell-enriched genes.

              Raquel del Toro, Claudia Prahst, Thomas Mathivet … (2010)
              Sprouting of developing blood vessels is mediated by specialized motile endothelial cells localized at the tips of growing capillaries. Following behind the tip cells, endothelial stalk cells form the capillary lumen and proliferate. Expression of the Notch ligand Delta-like-4 (Dll4) in tip cells suppresses tip cell fate in neighboring stalk cells via Notch signaling. In DLL4(+/-) mouse mutants, most retinal endothelial cells display morphologic features of tip cells. We hypothesized that these mouse mutants could be used to isolate tip cells and so to determine their genetic repertoire. Using transcriptome analysis of retinal endothelial cells isolated from DLL4(+/-) and wild-type mice, we identified 3 clusters of tip cell-enriched genes, encoding extracellular matrix degrading enzymes, basement membrane components, and secreted molecules. Secreted molecules endothelial-specific molecule 1, angiopoietin 2, and apelin bind to cognate receptors on endothelial stalk cells. Knockout mice and zebrafish morpholino knockdown of apelin showed delayed angiogenesis and reduced proliferation of stalk cells expressing the apelin receptor APJ. Thus, tip cells may regulate angiogenesis via matrix remodeling, production of basement membrane, and release of secreted molecules, some of which regulate stalk cell behavior.
              Article 0 comments Cited 174 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Arteriosclerosis, Thrombosis, and Vascular Biology
                Abbreviated Title: Arterioscler Thromb Vasc Biol.
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 1079-5642
                ISSN (Electronic): 1524-4636
                Publication date Created: November 2018
                Publication date (Print): November 2018
                Volume: 38
                Issue: 11
                Pages: 2550-2561
                Affiliations
                [1 ]From the Ludwig Institute for Cancer Research Ltd, Nuffield Department of Medicine (S.P., S.D.V.),University of Oxford, United Kingdom.
                [2 ]Department of Physiology, Anatomy and Genetics (S.D.V., A.N.),University of Oxford, United Kingdom.
                Article
                DOI: 10.1161/ATVBAHA.118.309669
                PMC ID: 6218004
                PubMed ID: 30354251
                SO-VID: 8be754bf-de13-40fa-8404-be77c926c88e
                Copyright © © 2018
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