Tcf3 promotes cell migration and wound repair through regulation of lipocalin 2

Qi Miao, Amy T. Ku, Yudai Nishino, Jeffrey M. Howard, Ajay S. Rao, Timothy M. Shaver, Gloria E. Garcia, Diep N. Le, Kristen L. Karlin, Thomas F. Westbrook, Valeria Poli and Hoang Nguyen ()
Additional contact information
Qi Miao: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Amy T. Ku: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Yudai Nishino: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Jeffrey M. Howard: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Ajay S. Rao: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Timothy M. Shaver: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Gloria E. Garcia: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Diep N. Le: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505
Kristen L. Karlin: Baylor College of Medicine, One Baylor Plaza, BCM 505
Thomas F. Westbrook: Baylor College of Medicine, One Baylor Plaza, BCM 505
Valeria Poli: Molecular Biotechnology Center, University of Turin, Via Nizza 52
Hoang Nguyen: Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, One Baylor Plaza, BCM 505

Nature Communications, 2014, vol. 5, issue 1, 1-15

Abstract: Abstract Cell migration is an integral part of re-epithelialization during skin wound healing, a complex process involving molecular controls that are still largely unknown. Here we identify a novel role for Tcf3, an essential transcription factor regulating embryonic and adult skin stem cell functions, as a key effector of epidermal wound repair. We show that Tcf3 is upregulated in skin wounds and that Tcf3 overexpression accelerates keratinocyte migration and skin wound healing. We also identify Stat3 as an upstream regulator of Tcf3. We show that the promigration effects of Tcf3 are non-cell autonomous and occur independently of its ability to interact with β-catenin. Finally, we identify lipocalin-2 as the key secreted factor downstream of Tcf3 that promotes cell migration in vitro and wound healing in vivo. Our findings provide new insights into the molecular controls of wound-associated cell migration and identify potential therapeutic targets for the treatment of defective wound repair.

Date: 2014
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DOI: 10.1038/ncomms5088

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