scholarly journals Activation of Wnt3a signaling stimulates intestinal epithelial repair by promoting c-Myc-regulated gene expression

2012 ◽  
Vol 302 (1) ◽  
pp. C277-C285 ◽  
Author(s):  
Lan Liu ◽  
Jaladanki N. Rao ◽  
Tongtong Zou ◽  
Lan Xiao ◽  
Alexis Smith ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cyclin E ◽  
Cell Renewal ◽  
Intestinal Epithelial ◽  
Epithelial Repair ◽  
Myc Gene ◽  
Factor C ◽  
Regulated Gene Expression

In response to mucosal injury, epithelial cells modify the patterns of expressed genes to repair damaged tissue rapidly. Our previous studies have demonstrated that the transcription factor c-Myc is necessary for stimulation of epithelial cell renewal during mucosal healing, but the up-stream signaling initiating c-Myc gene expression after injury remains unknown. Wnts are cysteine-rich glycoproteins that act as short-range ligands to locally activate receptor-mediated signaling pathways and correlate with the increased expression of the c-Myc gene. The current study tested the hypothesis that Wnt3a signaling is implicated in intestinal epithelial repair after wounding by stimulating c-Myc expression. Elevated Wnt3a signaling in intestinal epithelial cells (IEC-6 line) by coculturing with stable Wnt3a-transfected fibroblasts or ectopic overexpression of the Wnt3a gene enhanced intestinal epithelial repair after wounding. This stimulatory effect on epithelial repair was prevented by silencing the Wnt coreceptor LRP6 or by c-Myc silencing. Activation of the Wnt3a signaling pathway increased β-catenin nuclear translocation by decreasing its phosphorylation and stimulated c-Myc expression during epithelial repair after wounding. In stable Wnt3a-transfected IEC-6 cells, increased levels of c-Myc were associated with an increase in expression of c-Myc-regulated genes cyclcin D1 and cyclin E, whereas c-Myc silencing inhibited expression of cyclin D1 and cyclin E and delayed epithelial repair. These results indicate that elevated Wnt3a signaling in intestinal epithelial cells after wounding stimulates epithelial repair by promoting c-Myc-regulated gene expression.

scholarly journals IL-33 regulates gene expression in intestinal epithelial cells independently of its nuclear localization

2018 ◽  
Author(s):  
Zhengxiang He ◽  
Lili Chen ◽  
Glaucia C. Furtado ◽  
Sergio A. Lira
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Full Length ◽  
Nuclear Accumulation ◽  
List Type ◽  
Intestinal Epithelial ◽  
Regulated Gene Expression

AbstractIL-33 is a cytokine found in the extracellular space (mature IL-33) or in the cell nucleus (full-length IL-33). Nuclear accumulation of IL-33 has been reported in intestinal epithelial cells (IEC) during intestinal inflammation and cancer, but a functional role for this nuclear form remains unclear. To study the role of nuclear IL-33inIEC, we generated transgenic mice expressing full-length IL-33inthe intestinal epithelium (Vfl33mice). Expression of full-length IL-33 in the epithelium resulted in accumulation of IL-33 protein in the nucleus and secretion of IL-33. Over-expression of full-length IL-33 by IEC did not promote gut inflammation, but induced expression of genes in the IEC and lamina propria lymphocytes (LPL) that correlated negatively with genes expressed in inflammatory bowel diseases (IBD). Because the IL-33 receptor ST2 is expressed by IEC, there was the potential that both the mature and full-length forms could mediate this effect. To specifically interrogate the transcriptional role of nuclear IL-33,weintercrossed theVfl33mice with ST2-deficient mice. ST2 deficiency completely abrogated the transcriptional effects elicited by IL-33 expression, suggesting that the transcriptional effects of IL-33 on IEC are mediated by its mature, not its nuclear form.HighlightsExpression of full-length IL-33 in the epithelium resulted in accumulation of IL-33 protein in the nucleus and secretion of IL-33.Full-length IL-33 induced differential gene expression in IEC and LPL that was negatively associated with intestinal inflammatory diseasesIL-33 regulated gene expression in IEC via its extracellular (mature) form not via its nuclearform.

scholarly journals CDX2 regulates interleukin‐33 gene expression in intestinal epithelial cells (LS174T)

FEBS Open Bio ◽  
2021 ◽  
Author(s):  
Sylvester Larsen ◽  
Jakob Benedict Seidelin ◽  
Johanne Davidsen ◽  
Katja Dahlgaard ◽  
Claus Henrik Nielsen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Interleukin 33

GENE EXPRESSION IN INTESTINAL EPITHELIAL CELLS, IEC-6, IS ALTERED BY BURN INJURY-INDUCED CIRCULATING FACTORS

Shock ◽  
2001 ◽  
Vol 16 (4) ◽  
pp. 259-263 ◽  
Author(s):  
Maryam Varedi ◽  
Heung-Man Lee ◽  
George H. Greeley ◽  
David N. Herndon ◽  
Ella W. Englander
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Burn Injury ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Comparison of gene expression and activation of transcription factors in organoid-derived monolayer intestinal epithelial cells and organoids

2021 ◽  
Author(s):  
Yu Takahashi ◽  
Yu Inoue ◽  
Keitaro Kuze ◽  
Shintaro Sato ◽  
Makoto Shimizu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Gene Expression Regulation ◽  
Intestinal Epithelial Cells ◽  
Three Dimensional ◽  
Culture Conditions ◽  
Dependent Manner ◽  
Intestinal Epithelial

Abstract Intestinal organoids better represent in vivo intestinal properties than conventionally used established cell lines in vitro. However, they are maintained in three-dimensional culture conditions that may be accompanied by handling complexities. We characterized the properties of human organoid-derived two-dimensionally cultured intestinal epithelial cells (IECs) compared with those of their parental organoids. We found that the expression of several intestinal markers and functional genes were indistinguishable between monolayer IECs and organoids. We further confirmed that their specific ligands equally activate intestinal ligand-activated transcriptional regulators in a dose-dependent manner. The results suggest that culture conditions do not significantly influence the fundamental properties of monolayer IECs originating from organoids, at least from the perspective of gene expression regulation. This will enable their use as novel biological tools to investigate the physiological functions of the human intestine.

scholarly journals Endotoxin Increases Type II-Phospholipase A2 Gene Expression in Rat Intestinal Epithelial Cells

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 108A-108A
Author(s):  
Michael Amer ◽  
Yu Xiao ◽  
Luba Adler ◽  
Michael S Caplan
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Phospholipase A2 ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Type Ii

Influence of TNF-α on the gene expression profile in src transtormed intestinal epithelial cells

2001 ◽  
Vol 120 (5) ◽  
pp. A300 ◽  
Author(s):  
Naoki Kawai ◽  
Shingo Tsuji ◽  
Masahiko Tsujii ◽  
Masato Komori ◽  
Arata Kimura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Tnf Α

scholarly journals Alteration in Inflammatory Responses and Cytochrome P450 Expression of Porcine Jejunal Cells by Drinking Water Supplements

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Orsolya Palócz ◽  
Géza Szita ◽  
György Csikó
Keyword(s):  
Gene Expression ◽  
Drinking Water ◽  
Cytochrome P450 ◽  
Epithelial Cells ◽  
Fulvic Acid ◽  
Intestinal Epithelial Cells ◽  
Feed Additives ◽  
Feed Additive ◽  
Mrna Levels ◽  
Intestinal Epithelial

The intestinal epithelium is the first determining barrier to the drugs administered per os. Cytochrome P450 (CYP) enzymes are substantial in the initial step of xenobiotic metabolism; therefore, intestinal CYP enzyme activities could be an important influencing factor of the oral utilization of xenobiotic substances. In this study, the effect of four drinking water supplements on CYP mRNA levels of porcine intestinal epithelial cells was examined. Further goal of the study is to describe the effect of these feed additives on the proinflammatory response of the LPS-treated enterocytes. The nontransformed porcine intestinal epithelial cells (IPEC-J2) were grown on six-well polyester membrane inserts. Cell cultures were treated with LPS (10 μg/ml), β-glucan (5 and 50 μg/ml), sanguinarine-containing additive (5 and 50 μg/ml), drinking water acidifier (0.1 and 1 μl/ml), and fulvic acid (25 and 250 μg/ml) for 1 hour. Cells were washed with culture medium and incubated for additional 1 h before total RNA isolation. IL-6, IL-8, TNF-α, HSP70, CYP1A1, CYP1A2, and CYP3A29 mRNA levels were measured. The LPS treatment upregulated the gene expression of IL-8 and TNF-α. The relative gene expression of IL-6 remained unchanged and TNF-α and HSP70 were downregulated after the treatment with each feed additive. CYP1A1 and CYP1A2 expressions increased after sanguinarine-containing solution, fulvic acid, and drinking water acidifier treatment. None of the treatments changed the gene expression of CYP3A29, responsible for the metabolism of the majority of drug substances used in swine industry. The feed additive substances inhibited the expression of proinflammatory mediators HSP70 and TNF-α; however, β-glucan and fulvic acid elevated the production of the chemokine IL-8 mRNA in endotoxin-treated enterocytes. All acidic supplements increased the expression of CYP1A1 gene; their constituents may serve as a ligand of CYP1A1 nuclear receptors.

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