Arch Plast Surg Search

CLOSE


Arch Plast Surg > Volume 45(6); 2018 > Article
Yang, Moon, Kim, Lee, Yun, Lew, and Lee: Epithelial-mesenchymal transition in keloid tissue
Fibroblasts at the wound site are recognized as the primary drivers of scar formation. They differentiate into myofibroblasts, the key mediators of fibrosis, which are responsible for collagen deposition and wound contraction. Repair processes cease when epithelialization is completed in normal wounds, whereas in keloid wounds, they may continue and result in excessive accumulation of unorganized extracellular matrix, forming problematic scars.
In addition to resident mesenchymal cells, fibroblasts and myofibroblasts are thought to be derived from multiple sources, including epithelial-mesenchymal transition (EMT) [1]. During this process, epithelial cells experience intercellular and intracellular changes, including dissociation of junctional complexes, loss of apical-basolateral polarity, and repression of epithelial markers. As a result, epithelial cells lose many of their properties and take on characteristics of mesenchymal cells.
To investigate this process, an immunofluorescence assay using both epithelial and mesenchymal markers was performed using keloid tissues obtained from the anterior chest wall of a 70-year-old male patient (Fig. 1). After fixation, cells were incubated with primary antibodies against E-cadherin and vimentin (Abcam, Cambridge, UK), and subsequently labelled with fluorescently-tagged secondary antibodies. Counterstaining with 4’,6-diamidino-2-phenylindole (DAPI) (VECTOR Laboratories, Burlingame, CA, USA) was also performed.
Cells were visualized using an LSM 700 Carl Zeiss confocal microscope (Carl Zeiss MicroImaging, Thornwood, NY, USA). E-cadherin and vimentin expression were simultaneously observed at the dermo-epidermal junction in keloid tissue, indicating the occurrence of EMT (Fig. 2).
Although further investigations with additional keloid specimens are needed, we hope that our study yields some insight into the mechanisms of keloid formation.

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

Notes

Ethical approval

The study was approved by the Institutional Review Board of Yonsei University Medical Center (IRB No. 4-2017-0259) and performed in accordance with the principles of the Declaration of Helsinki. Written informed consent was obtained.

Notes

Patient consent

The patient provided written informed consent for the publication and the use of his image.

Fig. 1.
Patient with a keloid. A 70-year-old male with a keloid on the post-sternotomy area suffered from itchiness, pain, and skin tightening. The keloid was surgically excised intralesionally.
aps-2017-01214f1.tif
Fig. 2.
Epithelial-mesenchymal transition (EMT) characteristics in keloid tissue. (A) Expression of the epithelial marker E-cadherin (green) and (B) the mesenchymal marker vimentin (red) was observed via immunofluorescence. (C) DAPI counterstain of nuclei (blue). (D) Co-expression of E-cadherin and vimentin at the dermo-epidermal junction was observed, indicating the occurrence of the EMT process (A-D, magnification ×630).
aps-2017-01214f2.tif

Reference

1. Wynn TA. Cellular and molecular mechanisms of fibrosis. J Pathol 2008;214:199–210.
crossref pmid pmc
TOOLS
Share :
Facebook Twitter Linked In Google+ Line it
METRICS Graph View
  • 0 Crossref
  •   Scopus
  • 244 View
  • 21 Download


ABOUT
ARTICLE CATEGORY

Browse all articles >

BROWSE ARTICLES
AUTHOR INFORMATION
Editorial Office
101-2003, Lotte Castle President, 109, Mapodaero, Mapo-gu, Seoul 04146, Korea
Tel: +82-2-3472-8252    Fax: +82-2-3472-4254    E-mail: apsedit@gmail.com                

Copyright © 2018 by Korean Society of Plastic and Reconstructive Surgeons. All rights reserved.

Developed in M2community

Close layer
prev next