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Non-muscle myosin IIA differentially regulates intestinal epithelial cell restitution and matrix invasion
Epithelial Pathobiology Research Unit, the Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Epithelial Pathobiology Research Unit, the Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Epithelial Pathobiology Research Unit, the Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Laboratory of Molecular Cardiology, the National Heart, Lung, Blood Institute, National Institutes of Health, Bethesda, Maryland.
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2009 (English)In: American Journal of Pathology, ISSN 0002-9440, E-ISSN 1525-2191, Vol. 174, no 2, p. 436-448Article in journal (Refereed) Published
Abstract [en]

Epithelial cell motility is critical for self-rejuvenation of normal intestinal mucosa, wound repair, and cancer metastasis. This process is regulated by the reorganization of the F-actin cytoskeleton, which is driven by a myosin II motor. However, the role of myosin II in regulating epithelial cell migration remains poorly understood. This study addressed the role of non-muscle myosin (NM) IIA in two different modes of epithelial cell migration: two-dimensional (2-D) migration that occurs during wound closure and three-dimensional (3-D) migration through a Matrigel matrix that occurs during cancer metastasis. Pharmacological inhibition or siRNA-mediated knockdown of NM IIA in SK-CO15 human colonic epithelial cells resulted in decreased 2-D migration and increased 3-D invasion. The attenuated 2-D migration was associated with increased cell adhesiveness to collagen and laminin and enhanced expression of beta1-integrin and paxillin. On the 2-D surface, NM IIA-deficient SK-CO15 cells failed to assemble focal adhesions and F-actin stress fibers. In contrast, the enhanced invasion of NM IIA-depleted cells was dependent on Raf-ERK1/2 signaling pathway activation, enhanced calpain activity, and increased calpain-2 expression. Our findings suggest that NM IIA promotes 2-D epithelial cell migration but antagonizes 3-D invasion. These observations indicate multiple functions for NM IIA, which, along with the regulation of the F-actin cytoskeleton and cell-matrix adhesions, involve previously unrecognized control of intracellular signaling and protein expression.

Place, publisher, year, edition, pages
Elsevier, 2009. Vol. 174, no 2, p. 436-448
Keywords [en]
Animals, Blotting, Western, COS Cells, Cell Adhesion/*physiology, Cell Line, Tumor, Cell Movement/*physiology, Cercopithecus aethiops, Collagen, Drug Combinations, Fluorescent Antibody Technique, Humans, Immunohistochemistry, Intestinal Mucosa/*metabolism, Laminin, Microscopy, Confocal, Nonmuscle Myosin Type IIA/*metabolism, Proteoglycans, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction/*physiology, Wound Healing/physiology
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-141648DOI: 10.2353/ajpath.2009.080171ISI: 000262684800009PubMedID: 19147824Scopus ID: 2-s2.0-59649130347ISBN: 1525-2191 (Electronic) 0002-9440 (Linking) OAI: oai:DiVA.org:liu-141648DiVA, id: diva2:1149719
Note

Babbin, Brian A Koch, Stefan Bachar, Moshe Conti, Mary-Anne Parkos, Charles A Adelstein, Robert S Nusrat, Asma Ivanov, Andrei I eng K08 DK074706/DK/NIDDK NIH HHS/ R29 DK055679/DK/NIDDK NIH HHS/ DK 55679/DK/NIDDK NIH HHS/ DK 064399/DK/NIDDK NIH HHS/ DK 61379/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ DK 72564/DK/NIDDK NIH HHS/ R24 DK064399/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ DK 59888/DK/NIDDK NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ K08 DK074706-01/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2009/01/17 09:00 Am J Pathol. 2009 Feb;174(2):436-48. doi: 10.2353/ajpath.2009.080171. Epub 2009 Jan 15.

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

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