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Differential expression of interleukin-1/Toll-like receptor signaling regulators in microscopic and ulcerative colitis

Günaltay, Sezin, 1986- (author)
Örebro universitet,Institutionen för hälsovetenskap och medicin
Nyhlin, Nils, 1971- (author)
Örebro universitet,Institutionen för hälsovetenskap och medicin,Region Örebro län,Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden
Kumawat, Ashok Kumar, 1982- (author)
Örebro universitet,Institutionen för hälsovetenskap och medicin
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Tysk, Curt, 1949- (author)
Region Örebro län,Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden
Bohr, Johan, 1957- (author)
Örebro universitet,Institutionen för hälsovetenskap och medicin,Region Örebro län,Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden
Hultgren, Olof, 1970- (author)
Örebro universitet,Institutionen för läkarutbildning,Region Örebro län,Department of Microbiology and Immunology, Örebro University Hospital, Örebro, Sweden
Hultgren-Hörnquist, Elisabeth, 1965- (author)
Örebro universitet,Institutionen för läkarutbildning
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 (creator_code:org_t)
WJG Press, 2014
2014
English.
In: World Journal of Gastroenterology. - : WJG Press. - 1007-9327 .- 2219-2840. ; 20:34, s. 12249-12259
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • AIM: To investigate Toll-like receptor (TLR) signaling regulators in microscopic and ulcerative colitis patients.METHODS: Total RNA and microRNA were isolated from fresh frozen colonic biopsies of non-inflamed controls and patients with active or in-remission collagenous colitis (CC), lymphocytic colitis (LC), or ulcerative colitis (UC). We compared expressions of interleukin-1 receptor-associated kinase (IRAK)-2, IRAK-M, interleukin (IL)-37, microRNA (miR)-146a, miR-155, and miR-21 using quantitative real time reverse transcription polymerase chain reaction.RESULTS: IRAK-M expression was increased in LC patients with active disease in histopathological remission (LC-HR; P = 0.02) and UC patients (P = 0.01), but no differences in IRAK-2 expression were detected compared to controls. miR-146a, -155 and -21 expressions were increased in LC-HR (P = 0.04, 0.07, and 0.004) and UC (P = 0.02, 0.04 and 0.03) patients. miR-146a and miR-21 expressions were significantly enhanced in UC patients compared to UC remission (UC-R; P = 0.01 and 0.04). Likewise, active CC patients showed significantly increased expression of miR-155 (P = 0.003) and miR-21 (P = 0.006). IL-37 expression was decreased in both CC (P = 0.03) and LC (P = 0.04) patients with a similar trend in UC patients but not statistically significant, whilst it was increased in UC-R patients compared to controls (P = 0.02) and active UC (P = 0.001).CONCLUSION: The identification of differentially expressed miRNAs, IL-37, and IRAK-M suggests different pathophysiologic mechanisms in various disease stages in LC, CC, and UC. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Gastroenterologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Gastroenterology and Hepatology (hsv//eng)

Keyword

Interleukin-37
MicroRNA
Lymphocytic colitis
Collagenous colitis
Ulcerative colitis

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