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Type: Journal article
Title: Tropomyosin regulates cell migration during skin wound healing
Author: Lees, J.
Ching, Y.
Adams, D.
Bach, C.
Samuel, M.
Kee, A.
Hardeman, E.
Gunning, P.
Cowin, A.
O'Neill, G.
Citation: Journal of Investigative Dermatology, 2013; 133(5):1330-1339
Publisher: Blackwell Publishing Inc
Issue Date: 2013
ISSN: 0022-202X
Statement of
Justin G. Lees, Yu Wooi Ching, Damian H. Adams, Cuc T.T. Bach, Michael S. Samuel, Anthony J. Kee, Edna C. Hardeman, Peter Gunning, Allison J. Cowin and Geraldine M. O’Neill
Abstract: Precise orchestration of actin polymer into filaments with distinct characteristics of stability, bundling, and branching underpins cell migration. A key regulator of actin filament specialization is the tropomyosin family of actin-associating proteins. This multi-isoform family of proteins assemble into polymers that lie in the major groove of polymerized actin filaments, which in turn determine the association of molecules that control actin filament organization. This suggests that tropomyosins may be important regulators of actin function during physiological processes dependent on cell migration, such as wound healing. We have therefore analyzed the requirement for tropomyosin isoform expression in a mouse model of cutaneous wound healing. We find that mice in which the 9D exon from the TPM3/γTm tropomyosin gene is deleted (γ9D -/-) exhibit a more rapid wound-healing response 7 days after wounding compared with wild-type mice. Accelerated wound healing was not associated with increased cell proliferation, matrix remodeling, or epidermal abnormalities, but with increased cell migration. Rac GTPase activity and paxillin phosphorylation are elevated in cells from γ9D -/- mice, suggesting the activation of paxillin/Rac signaling. Collectively, our data reveal that tropomyosin isoform expression has an important role in temporal regulation of cell migration during wound healing.
Keywords: Cells, Cultured; Cell Line, Tumor; Extracellular Matrix; Skin; Animals; Mice, Inbred C57BL; Mice, Transgenic; Mice, Knockout; Mice; rac GTP-Binding Proteins; Tropomyosin; Models, Animal; Wound Healing; Signal Transduction; Cell Proliferation; Cell Movement; Phosphorylation; Female; Paxillin
Rights: © 2013 The Society for Investigative Dermatology
RMID: 0020126107
DOI: 10.1038/jid.2012.489
Grant ID:
Appears in Collections:Molecular and Biomedical Science publications

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