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Epithelial-Mesenchymal Transition, TGF-beta, and Osteopontin in Wound Healing and Tissue Remodeling After Injury

Department of Surgery, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Journal of burn care & research: official publication of the American Burn Association (Impact Factor: 1.55). 05/2012; 33(3):311-8. DOI: 10.1097/BCR.0b013e318240541e
Source: PubMed

ABSTRACT Epithelial-mesenchymal transition (EMT) is a process essential to wound healing and tissue remodeling after a thermal burn or other injury. EMT is characterized by phenotypic changes in epithelial cells that render them apolar, with decreased cell-cell adhesions, increased motility, and changes in cytoskeletal architecture similar to mesenchymal stem cells. With regard to healing a thermal burn wound, many facets of wound healing necessitate cells to undergo these phenotypic changes; two will be described in the following review. The first is the differentiation of epithelial cells into myofibroblasts that rebuild the extracellular matrix and facilitate wound contraction. The second is reepithelialization by keratinocytes. The primary cytokine signal identified in the literature that triggers EMT is transforming growth factor (TGF)-β. In addition to its vital role in the induction of EMT, TGF-β has many other roles in the wound healing process. The following review will provide evidence that EMT is a central event in wound healing. It will also show the importance of a regulated amount of TGF-β for proper wound healing. Finally, osteopontin will be briefly discussed with its relation to wound healing and its connections to EMT and TGF-β.

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    • "Although considerable progress has been made towards understanding the etiology of the disease, the pathogenesis of pterygium is not completely understood (Bradley et al., 2008; Chui et al., 2008). EMT is critical in both developmental processes (Bolender and Markwald, 1979; Duband et al., 1995; Griffith and Hay, 1992; Viebahn, 1995), wound healing and tissue remodeling (Weber et al., 2012), and tumor metastasis (Thiery et al., 2009) and describes a reversible series of events during which epithelial cells lose cellecell contacts and acquire mesenchymal characteristics (Gregory et al., 2008b). These events involve molecular reprogramming of the cell, including loss or redistribution of epithelial-specific cellecell adhesion molecules such as E-cadherin, and turning on of mesenchymal markers including fibronectin, vimentin and N-cadherin (Thiery and Sleeman, 2006). "
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