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    Mice overexpressing CD97 in intestinal epithelial cells provide a unique model for mammalian postnatal intestinal cylindrical growth (2013)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Aust, Gabriela
    Kerner, Christiane
    Gonsior, Susann
    Sittig, Doreen
    Schneider, Hartmut
    Buske, Peter
    Scholz, Markus
    Dietrich, Norman
    Oldenburg, Sindy
    Karpus, Olga N
    Galle, Jörg
    Amasheh, Salah (WE 2)
    Hamann, Jörg
    Quelle
    Molecular biology of the cell; 24(14) — S. 2256–2268
    ISSN: 1059-1524
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://edocs.fu-berlin.de/docs/receive/FUDOCS_document_000000022588
    DOI: 10.1091/mbc.E13-04-0175
    Pubmed: 23676664
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    Institut für Veterinär-Physiologie

    Oertzenweg 19 b
    14163 Berlin
    Tel.+49 30 838 62600 Fax.+49 30 838-62610
    email:physiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Postnatal enlargement of the mammalian intestine comprises cylindrical and luminal growth, associated with crypt fission and crypt/villus hyperplasia, respectively, which subsequently predominate before and after weaning. The bipartite adhesion G protein-coupled receptor CD97 shows an expression gradient along the crypt-villus axis in the normal human intestine. We here report that transgenic mice overexpressing CD97 in intestinal epithelial cells develop an upper megaintestine. Intestinal enlargement involves an increase in length and diameter but does not affect microscopic morphology, as typical for cylindrical growth. The megaintestine is acquired after birth and before weaning, independent of the genotype of the mother, excluding altered availability of milk constituents as driving factor. CD97 overexpression does not regulate intestinal growth factors, stem cell markers, and Wnt signaling, which contribute to epithelial differentiation and renewal, nor does it affect suckling-to-weaning transition. Consistent with augmented cylindrical growth, suckling but not adult transgenic mice show enlarged crypts and thus more crypt fissions caused by a transient increase of the crypt transit-amplifying zone. Intestinal enlargement by CD97 requires its seven-span transmembrane/cytoplasmic C-terminal fragment but not the N-terminal fragment binding partner CD55. In summary, ectopic expression of CD97 in intestinal epithelial cells provides a unique model for intestinal cylindrical growth occurring in breast-fed infants.