Inflammatory gene signature in ulcerative colitis with cDNA macroarray analysis

Okahara, Satoshi; Arimura, Yoshiaki; Yabana, Takashi; Kobayashi, Katsuaki; Gotoh, Akito; Motoya, Satoshi; Imamura, Akira; Endo, Takao; Imai, Kazushi

doi:10.1111/j.1365-2036.2005.02443.x

Cited by 48 publications

(27 citation statements)

References 41 publications

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“…The expression of lipocalin-2 was not different among treatments in the chronic model, and it may be because it has been used as a marker of neutrophil inflammation in conditions such as ulcerative colitis and proctitis. 19 Histological analysis of bladder sections demonstrated the presence of neutrophils in the acute model but very few or none in the chronic model. Lipocalin-2 expression in ovariectomized mice treated with 17␤-estradiol was slightly increased when compared with control mice as reported previously in the uterus.…”

Section: Discussionmentioning

confidence: 96%

Role of Nicotinic and Estrogen Signaling during Experimental Acute and Chronic Bladder Inflammation

Martínez‐Ferrer

Iturregui

Uwamariya

et al. 2008

The American Journal of Pathology

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Inflammation is a physiological process that characterizes many bladder diseases. We hypothesized that nicotinic and estrogen signaling could down-regulate bladder inflammation. Cyclophosphamide was used to induce acute and chronic bladder inflammation. Changes in bladder inflammation were measured histologically and by inflammatory gene expression. Antagonizing nicotinic signaling with mecamylamine further aggravated acute and chronic inflammatory changes resulting from cyclophosphamide treatment. Estrogen and nicotinic signaling independently attenuated acute bladder inflammation by decreasing neutrophil recruitment and down-regulating elevated lipocalin-2 and cathepsin D expression. However, the combined signaling by the estrogen and nicotinic pathways, as measured by macrophage infiltration and up-regulation of interleukin-6 expression in the bladder, synergistically reduced chronic bladder inflammation. The elevated expression of p65 nuclear localization in bladders treated with cyclophosphamide or cyclophosphamide with mecamylamine suggested nuclear factor-B activation in the chronic inflammatory process. The complementary treat-ment of 17␤-estradiol and the nicotinic agonist anabasine resulted in the translocation of p65 to the cytoplasm, again greater than either alone. Activation of nuclear factor-B can result in macrophage activation and/or elevation in epithelial proliferation. These data suggest that 17␤-estradiol and anabasine reduce chronic bladder inflammation through reduction of nuclear translocation of p65 to suppress cytokine expression. (Am J

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Section: Discussionmentioning

confidence: 96%

Role of Nicotinic and Estrogen Signaling during Experimental Acute and Chronic Bladder Inflammation

Martínez‐Ferrer

Iturregui

Uwamariya

et al. 2008

The American Journal of Pathology

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“…3), suggesting that this network may be correlated with the colonic cell differentiation induced by SB. Indeed, PMP22 [29], RB1 [30], NDRG1 [31], IGF2R [32], IGF2 [33], JUNB [34], TIMP1 [35] and THRA [36] have been reported to be expressed in the small intestine or colon. This network includes IGF2 at its center.…”

Section: Discussionmentioning

confidence: 99%

Genetic networks responsive to sodium butyrate in colonic epithelial cells

et al. 2006

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We performed microarray and computational gene network analyses to identify the detailed mechanisms by which sodium butyrate (SB) induces cell growth arrest and the differentiation of mouse colonic epithelial MCE301 cells. Two thousand six hundred four differentially expressed probe sets were identified in the cells treated with 2 mM SB and were classified into four groups. Of these, the gradually increased group and the gradually and remarkably decreased group contained the genetic networks for cellular development and cell cycles or canonical pathways for fatty acid biosynthesis and pyrimidine metabolism, respectively. The present results provide a basis for understanding the detailed molecular mechanisms of action of SB in colonic epithelial cells.

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“…Genes encoding for chemokines, markers of neutrophil activation, and anti-inflammatory factors are upregulated in humans with CE. 11,12 Moreover, disturbances in expression of genes encoding for proteins involved in innate or adaptive immunity, detoxification, and nuclear transcription are important in the pathogenesis of mucosal inflammation in mice with experimentally induced colitis. 13,14 The objectives of the study reported here were to determine gastrointestinal mucosal gene expression patterns in dogs with CE, compare results with those for healthy control dogs, and determine whether gene expression differs among dogs with CE of various severities.…”

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confidence: 99%

Gene expression in intestinal mucosal biopsy specimens obtained from dogs with chronic enteropathy

Wilke¹,

Nettleton²,

Wymore³

et al. 2012

ajvr

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Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE). Animals—18 dogs with CE and 6 healthy control dogs. Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed. Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis. Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity. Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease.

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Inflammatory gene signature in ulcerative colitis with cDNA macroarray analysis

Cited by 48 publications

References 41 publications

Role of Nicotinic and Estrogen Signaling during Experimental Acute and Chronic Bladder Inflammation

Role of Nicotinic and Estrogen Signaling during Experimental Acute and Chronic Bladder Inflammation

Genetic networks responsive to sodium butyrate in colonic epithelial cells

Gene expression in intestinal mucosal biopsy specimens obtained from dogs with chronic enteropathy

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