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MBC in Press, published online ahead of print June 7, 2006
Mol. Biol. Cell 10.1091/mbc.E06-02-0102

A more recent version of this article appeared on August 1, 2006
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Submitted on February 6, 2006
Revised on May 15, 2006
Accepted on May 25, 2006

A Role for the MEK Kinase 1 in Epithelial Wound Healing

Maoxian Deng,*{dagger} Wei-Li Chen,{dagger}{ddagger}{sect} Atsushi Takatori,* Zhimin Peng,* Lin Zhang,*|| Maureen Mongan,* Ranjani Parthasarathy,* Maureen Sartor,* Marian Miller,* Jianhua Yang,¶ Bing Su,¶ Winston W.-Y. Kao,{sect} and Ying Xia*{sect}

*Department of Environmental Health and Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH 45267-0056; {ddagger}Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan, ROC; {sect}Department of Ophthalmology, University of Cincinnati Medical Center, Cincinnati, OH 45267; ||Department of Central Lab, Southern Medical University, Tonghe, Guangzhou, People’s Republic of China; Department of Immunology, M. D. Anderson Cancer Center, The University of Texas, Houston, TX 77030

Monitoring Editor: J. Silvio Gutkind

The MEK kinase 1 (MEKK1) mediates activin B signals required for eyelid epithelium morphogenesis during mouse fetal development. The present studies investigate the role of MEKK1 in epithelial wound healing, another activin-regulated biological process. In a skin wound model, injury markedly stimulates MEKK1 expression and activity, which are in turn required for the expression of genes involved in extracellular matrix (ECM) homeostasis. MEKK1 ablation or down-regulation by interfering RNA (iRNA) significantly delays skin wound closure and impairs activation of Jun N-terminal kinases (JNKs), induction of plasminogen activator inhibitor-1 (PAI-1) and restoration of cell-cell junctions of the wounded epidermis. Conversely, expression of wild type MEKK1 accelerates reepithelialization of full-thickness skin and corneal debridement wounds by mechanisms involving epithelial cell migration, a cell function that is partially abolished by neutralizing antibodies for PAI-1 and metalloproteinase III (MMP-3). Our data suggest that MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in ECM homeostasis, epithelial cell migration and wound reepithelialization.

{dagger}These authors contributed equally to this work.

Address correspondence to: Ying Xia (xiay{at}email.uc.edu)




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