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The epithelial mesenchymal transition process may contribute to the pathogenesis of amniotic band syndrome.

Abstract
The etiology of the amniotic band syndrome is unknown, and has been subject of debate since the time of Hippocrates. The most accepted theories fail to cover all the abnomalities found in affected children. During organogenesis the epithelial-mesenchymal transition process (EMTP) participates in adequate formation of different organs from three embryo layers. Altered activation of EMTP occurs when the epithelial homeostasis is disturbed, the resulting myofibroblasts are able to secrete extracellular matrix proteins and deposit them on the tissues contributing to a fibrotic phenotype. If injury occurs during organogenesis, wound healing could be exaggerated and fibrotic response could be triggered. The molecule that regulates both of these processes (EMTP and fibrosis) is the transforming growth factor β (TGFβ); indeed null animals for TGFβ isoforms show similar defects than those seen in the amniotic band syndrome. Based on documented evidence this review intends to explain how the epithelial mesenchymal transition process may contribute to the pathogenesis of amniotic band syndrome.
AuthorsM Romero-Valdovinos, N Bobadilla-Sandoval, A Flisser, F Vadillo-Ortega
JournalMedical hypotheses (Med Hypotheses) Vol. 83 Issue 3 Pg. 306-11 (Sep 2014) ISSN: 1532-2777 [Electronic] United States
PMID24998668 (Publication Type: Journal Article)
CopyrightCopyright © 2014 Elsevier Ltd. All rights reserved.
Chemical References
  • Transforming Growth Factor beta
  • Wnt Proteins
  • Fibroblast Growth Factors
Topics
  • Amnion (metabolism)
  • Amniotic Band Syndrome (physiopathology)
  • Epithelial Cells (metabolism)
  • Epithelial-Mesenchymal Transition
  • Female
  • Fibroblast Growth Factors (metabolism)
  • Fibroblasts (metabolism)
  • Fibrosis (physiopathology)
  • Homeostasis
  • Humans
  • Infant, Newborn
  • Mutation
  • Organogenesis
  • Phenotype
  • Pregnancy
  • Signal Transduction
  • Transforming Growth Factor beta (metabolism)
  • Wnt Proteins (metabolism)

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