Elevated Expression of AXL May Contribute to the Epithelial-to- Mesenchymal Transition in Inflammatory Bowel Disease Patients

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...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Boros Éva
Kellermayer Zoltán
Balogh Péter
Strifler Gerda
Vörös Andrea
Sarlós Patrícia
Vincze Áron
Varga Csaba
Nagy István
Dokumentumtípus: Cikk
Megjelent: 2018
Sorozat:MEDIATORS OF INFLAMMATION 2018
doi:10.1155/2018/3241406

mtmt:3397951
Online Access:http://publicatio.bibl.u-szeged.hu/16036
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245 1 0 |a Elevated Expression of AXL May Contribute to the Epithelial-to- Mesenchymal Transition in Inflammatory Bowel Disease Patients  |h [elektronikus dokumentum] /  |c  Boros Éva 
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300 |a Paper 3241406-11 p 
490 0 |a MEDIATORS OF INFLAMMATION  |v 2018 
520 3 |a 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. 
700 0 1 |a Kellermayer Zoltán  |e aut 
700 0 1 |a Balogh Péter  |e aut 
700 0 1 |a Strifler Gerda  |e aut 
700 0 1 |a Vörös Andrea  |e aut 
700 0 1 |a Sarlós Patrícia  |e aut 
700 0 1 |a Vincze Áron  |e aut 
700 0 1 |a Varga Csaba  |e aut 
700 0 1 |a Nagy István  |e aut 
856 4 0 |u http://publicatio.bibl.u-szeged.hu/16036/1/Strifler2018-Hindawi-Morahalom.pdf  |z Dokumentum-elérés