Elevated expression of AXL may contribute to the epithelial-to-mesenchymal transition in inflammatory bowel disease patients

Éva Boros, Zoltán Kellermayer, Péter Balogh, Gerda Strifler, Andrea Vörös, Patrícia Sarlós, Áron Vincze, Csaba Varga, István Nagy

Research output: Article

1 Citation (Scopus)

Abstract

Understanding the molecular mechanisms inducing and regulating epithelial-to-mesenchymal transition (EMT) upon chronic intestinal inflammation is critical for understanding the exact pathomechanism of inflammatory bowel disease (IBD). The aim of this study was to determine the expression profile of TAM family receptors in an inflamed colon. For this, we used a rat model of experimental colitis and also collected samples from colons of IBD patients. Samples were taken from both inflamed and uninflamed regions of the same colon; the total RNA was isolated, and the mRNA and microRNA expressions were monitored. We have determined that AXL is highly induced in active-inflamed colon, which is accompanied with reduced expression of AXL-regulating microRNAs. In addition, the expression of genes responsible for inducing or maintaining mesenchymal phenotype, such as SNAI1, ZEB2, VIM, MMP9, and HIF1α, were all significantly induced in the active-inflamed colon of IBD patients while the epithelial marker E-cadherin (CDH1) was downregulated. We also show that, in vitro, monocytic and colonic epithelial cells increase the expression of AXL in response to LPS or TNFα stimuli, respectively. In summary, we identified several interacting genes and microRNAs with mutually exclusive expression pattern in active-inflamed colon of IBD patients. Our results shed light onto a possible AXL- and microRNA-mediated regulation influencing epithelial-to-mesenchymal transition in IBD.

Original languageEnglish
Article number3241406
JournalMediators of inflammation
Volume2018
DOIs
Publication statusPublished - 2018

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

Fingerprint Dive into the research topics of 'Elevated expression of AXL may contribute to the epithelial-to-mesenchymal transition in inflammatory bowel disease patients'. Together they form a unique fingerprint.

  • Cite this