title: Role of Altered Expression of miR-146a, miR-155, and miR-122 in Pediatric Patients with Inflammatory Bowel Disease.
abstract: BACKGROUND
  Evidence suggests the central role of tumor necrosis factor (TNF)-α in the pathomechanism of inflammatory bowel disease (IBD); however, its effect on epigenetic factors, including small non-coding microRNAs (miRs), is less known. Our present aim was the comparative investigation of the expression of TNF-α and immune response-related miRs in children with Crohn's disease (CD) and ulcerative colitis (UC).
  
  
  METHODS
  Fresh-frozen (FF) and formalin-fixed, paraffin-embedded (FFPE) biopsies were used to analyze the expression of miR-146a, -155, -122, and TNF-α by real-time reverse transcription polymerase chain reaction in macroscopically inflamed (CD: 12 FFPE and 24 FF; UC: 10 FF) and intact (CD: 12 FFPE; 14 FF) colonic biopsies of children with IBD and controls (16 FFPE; 23 FF). The expression of miR-146a, -155, and -122 was also determined in TNF-α-treated HT-29 colonic epithelial cells.
  
  
  RESULTS
  Increased expression of TNF-α was observed in the colonic mucosa of children with CD and UC in comparison with controls. Expression of miR-146a and -155 was higher in the inflamed mucosa of children with CD and UC than in the intact mucosa. Expression of miR-122 elevated in the macroscopically intact colonic regions of CD compared with controls and patients with UC. In HT-29 cells, TNF-α treatment increased the expression of miR-146a and -155, but not that of miR-122.
  
  
  CONCLUSIONS
  Our results showed altered expression of miR-146a, -155, and -122 in the colonic mucosa of children with IBD and in TNF-α-treated colonic epithelial cells. Our data suggest the TNF-α-related involvement of these miRs in the pathogenesis of IBD.
authors.affiliation: *1st Department of Pediatrics, Semmelweis University, Budapest, Hungary; †2nd Department of Internal Medicine, Semmelweis University, Budapest, Hungary; ‡Department of Pediatrics and Pediatric Health Care Center, University of Szeged, Szeged, Hungary; §2nd Department of Pathology, Semmelweis University, Budapest, Hungary; ‖MTA-SE, Tumor Progression Research Group, Budapest, Hungary; and ¶MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary.
authors.forename: Nóra J
authors.initials: NJ
authors.lastname: Béres
authors.forename: Dolóresz
authors.initials: D
authors.lastname: Szabó
authors.forename: Dorottya
authors.initials: D
authors.lastname: Kocsis
authors.forename: Dániel
authors.initials: D
authors.lastname: Szűcs
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Kiss
authors.forename: Katalin E
authors.initials: KE
authors.lastname: Müller
authors.forename: Gábor
authors.initials: G
authors.lastname: Lendvai
authors.forename: András
authors.initials: A
authors.lastname: Kiss
authors.forename: András
authors.initials: A
authors.lastname: Arató
authors.forename: Erna
authors.initials: E
authors.lastname: Sziksz
authors.forename: Ádám
authors.initials: Á
authors.lastname: Vannay
authors.forename: Attila J
authors.initials: AJ
authors.lastname: Szabó
authors.forename: Gábor
authors.initials: G
authors.lastname: Veres
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D002648:Child; D003093:Colitis, Ulcerative / Q000235:genetics* / Q000473:pathology; D003424:Crohn Disease / Q000235:genetics* / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D019073:HT29 Cells; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics*; D011379:Prognosis; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: C531907:MIRN122 microRNA, human; C542542:MIRN146 microRNA, human; C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha