TY - JOUR
T1 - Epithelial-mesenchymal transition in tissue repair and fibrosis
AU - Stone, Rivka C.
AU - Pastar, Irena
AU - Ojeh, Nkemcho
AU - Chen, Vivien
AU - Liu, Sophia
AU - Garzon, Karen I.
AU - Tomic-Canic, Marjana
N1 - Funding Information:
Our research is supported by the National Institutes of Health grants NR015649, NR013881, and DK098055.
Publisher Copyright:
© 2016, Springer-Verlag Berlin Heidelberg.
PY - 2016/9/1
Y1 - 2016/9/1
N2 - The epithelial-mesenchymal transition (EMT) describes the global process by which stationary epithelial cells undergo phenotypic changes, including the loss of cell-cell adhesion and apical-basal polarity, and acquire mesenchymal characteristics that confer migratory capacity. EMT and its converse, MET (mesenchymal-epithelial transition), are integral stages of many physiologic processes and, as such, are tightly coordinated by a host of molecular regulators. Converging lines of evidence have identified EMT as a component of cutaneous wound healing, during which otherwise stationary keratinocytes (the resident skin epithelial cells) migrate across the wound bed to restore the epidermal barrier. Moreover, EMT plays a role in the development of scarring and fibrosis, as the matrix-producing myofibroblasts arise from cells of the epithelial lineage in response to injury but are pathologically sustained instead of undergoing MET or apoptosis. In this review, we summarize the role of EMT in physiologic repair and pathologic fibrosis of tissues and organs. We conclude that further investigation into the contribution of EMT to the faulty repair of fibrotic wounds might identify components of EMT signaling as common therapeutic targets for impaired healing in many tissues. [Figure not available: see fulltext.]
AB - The epithelial-mesenchymal transition (EMT) describes the global process by which stationary epithelial cells undergo phenotypic changes, including the loss of cell-cell adhesion and apical-basal polarity, and acquire mesenchymal characteristics that confer migratory capacity. EMT and its converse, MET (mesenchymal-epithelial transition), are integral stages of many physiologic processes and, as such, are tightly coordinated by a host of molecular regulators. Converging lines of evidence have identified EMT as a component of cutaneous wound healing, during which otherwise stationary keratinocytes (the resident skin epithelial cells) migrate across the wound bed to restore the epidermal barrier. Moreover, EMT plays a role in the development of scarring and fibrosis, as the matrix-producing myofibroblasts arise from cells of the epithelial lineage in response to injury but are pathologically sustained instead of undergoing MET or apoptosis. In this review, we summarize the role of EMT in physiologic repair and pathologic fibrosis of tissues and organs. We conclude that further investigation into the contribution of EMT to the faulty repair of fibrotic wounds might identify components of EMT signaling as common therapeutic targets for impaired healing in many tissues. [Figure not available: see fulltext.]
KW - Dermal fibroblasts
KW - Epithelial-mesenchymal transition
KW - Fibrosis
KW - Keratinocytes
KW - Wound healing
UR - http://www.scopus.com/inward/record.url?scp=84979656048&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84979656048&partnerID=8YFLogxK
U2 - 10.1007/s00441-016-2464-0
DO - 10.1007/s00441-016-2464-0
M3 - Review article
C2 - 27461257
AN - SCOPUS:84979656048
VL - 365
SP - 495
EP - 506
JO - Zeitschrift für Zellforschung und mikroskopische Anatomie (Vienna, Austria : 1948)
JF - Zeitschrift für Zellforschung und mikroskopische Anatomie (Vienna, Austria : 1948)
SN - 0302-766X
IS - 3
ER -