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Dkk-1 inhibits intestinal epithelial cell migration by attenuating directional polarization of leading edge cells
Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
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2009 (English)In: Molecular Biology of the Cell, ISSN 1059-1524, E-ISSN 1939-4586, Vol. 20, no 22, p. 4816-4825Article in journal (Refereed) Published
Abstract [en]

Wnt signaling pathways regulate proliferation, motility, and survival in a variety of human cell types. Dickkopf-1 (Dkk-1) is a secreted Wnt antagonist that has been proposed to regulate tissue homeostasis in the intestine. In this report, we show that Dkk-1 is secreted by intestinal epithelial cells after wounding and that it inhibits cell migration by attenuating the directional orientation of migrating epithelial cells. Dkk-1 exposure induced mislocalized activation of Cdc42 in migrating cells, which coincided with a displacement of the polarity protein Par6 from the leading edge. Consequently, the relocation of the microtubule organizing center and the Golgi apparatus in the direction of migration was significantly and persistently inhibited in the presence of Dkk-1. Small interfering RNA-induced down-regulation of Dkk-1 confirmed that extracellular exposure to Dkk-1 was required for this effect. Together, these data demonstrate a novel role of Dkk-1 in the regulation of directional polarization of migrating intestinal epithelial cells, which contributes to the effect of Dkk-1 on wound closure in vivo.

Place, publisher, year, edition, pages
Bethesda, United States: American Society for Cell Biology , 2009. Vol. 20, no 22, p. 4816-4825
Keyword [en]
Adaptor Proteins, Signal Transducing/genetics/metabolism, Animals, Apoptosis/physiology, Caco-2 Cells, Cell Movement/*physiology, *Cell Polarity, Cell Proliferation, *Epithelial Cells/cytology/physiology, Golgi Apparatus/metabolism, Humans, Intercellular Signaling Peptides and Proteins/genetics/*metabolism, Intestinal Mucosa/cytology, Microtubule-Organizing Center/metabolism, Wnt Proteins/genetics/metabolism, cdc42 GTP-Binding Protein/genetics/metabolism
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-141658DOI: 10.1091/mbc.E09-05-0415ISI: 000271769900017PubMedID: 19776352Scopus ID: 2-s2.0-73949114462ISBN: 1939-4586 (Electronic) 1059-1524 (Linking) OAI: oai:DiVA.org:liu-141658DiVA, id: diva2:1149714
Note

Koch, Stefan Capaldo, Christopher T Samarin, Stanislav Nava, Porfirio Neumaier, Irmgard Skerra, Arne Sacks, David B Parkos, Charles A Nusrat, Asma eng R01 DK079392/DK/NIDDK NIH HHS/ R29 DK055679/DK/NIDDK NIH HHS/ DK-72564/DK/NIDDK NIH HHS/ DK-055679/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ DK-61379/DK/NIDDK NIH HHS/ DK-79392/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural 2009/09/25 06:00 Mol Biol Cell. 2009 Nov;20(22):4816-25. doi: 10.1091/mbc.E09-05-0415. Epub 2009 Sep 23.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved

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