scholarly journals miR-30 Family Controls Proliferation and Differentiation of Intestinal Epithelial Cell Models by Directing a Broad Gene Expression Program That Includes SOX9 and the Ubiquitin Ligase Pathway

2016 ◽  
Vol 291 (31) ◽  
pp. 15975-15984 ◽  
Author(s):  
Bailey C. E. Peck ◽  
John Sincavage ◽  
Sydney Feinstein ◽  
Amanda T. Mah ◽  
James G. Simmons ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Ubiquitin Ligase ◽  
Intestinal Epithelial Cell ◽  
Gene Expression Program ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
Proliferation And Differentiation ◽  
Expression Program

Lipid Composition of Liposomal Membrane Largely Affects Its Transport and Uptake through Small Intestinal Epithelial Cell Models

Lipids ◽  
2020 ◽  
Vol 55 (6) ◽  
pp. 671-682 ◽  
Author(s):  
Keisuke Konishi ◽  
Lei Du ◽  
Grégory Francius ◽  
Michel Linder ◽  
Tomoaki Sugawara ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Lipid Composition ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
Liposomal Membrane ◽  
Small Intestinal Epithelial Cell ◽  
Small Intestinal

scholarly journals Different Sources of Copper Effect on Intestinal Epithelial Cell: Toxicity, Oxidative Stress, and Metabolism

Metabolites ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 11
Author(s):  
Runxian Li ◽  
Yang Wen ◽  
Gang Lin ◽  
Chengzhen Meng ◽  
Pingli He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Epithelial Cell ◽  
Protein Expression ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial ◽  
Protein Expression Level ◽  
Treatment Groups ◽  
All Treatment

Copper (Cu) is widely used in the swine industry to improve the growth performance of pigs. However, high doses of copper will induce cell damage and toxicity. The aim of this study was to evaluate toxicity, bioavailability, and effects on metabolic processes of varying copper sources using porcine intestinal epithelial cells (IPEC-J2) as a model. The IPEC-J2 were treated with two doses (30 and 120 μM) of CuSO4, Cu Glycine (Cu-Gly), and Cu proteinate (Cu-Pro) for 10 h, respectively. Cell damage and cellular copper metabolism were measured by the changes in cell viability, copper uptake, oxidative stress biomarkers, and gene/protein expression levels. The results showed that cell viability and ratio of reduced and oxidized glutathione (GSH/GSSG) decreased significantly in all treatment groups; intracellular copper content increased significantly in all treatment groups; total superoxide dismutase (SOD) activity increased significantly in the 120 μM exposed groups; SOD1 protein expression levels were significantly upregulated in 30 μM Cu-Pro, 120 μM Cu-Gly, and 120 μM Cu-Pro treatment groups; intracellular reactive oxygen species (ROS) generation and malondialdehyde (MDA) content increased significantly in 30 μM treatment groups and 120 μM CuSO4 treatment group. CTR1 and ATP7A gene expression were significantly downregulated in the 120 μM exposed groups. While upregulation of ATOX1 expression was observed in the presence of 120 μM Cu-Gly and Cu-Pro. ASCT2 gene expression was significantly upregulated after 120 μM Cu-Glycine and CuSO4 exposure, and PepT1 gene expression was significantly upregulated after Cu-Pro exposure. In addition, CTR1 protein expression level decreased after 120 μM CuSO4 and Cu-Gly exposure. PepT1 protein expression level was only upregulated after 120 μM Cu-Pro exposure. These findings indicated that extra copper supplementation can induce intestinal epithelial cell injury, and different forms of copper may have differing effects on cell metabolism.

scholarly journals Transport and uptake effects of marine complex lipid liposomes in small intestinal epithelial cell models

2016 ◽  
Vol 7 (4) ◽  
pp. 1904-1914 ◽  
Author(s):  
Lei Du ◽  
Yu-Hong Yang ◽  
Jie Xu ◽  
Yu-Ming Wang ◽  
Chang-Hu Xue ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Monolayer ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
M Cell ◽  
Small Intestinal Epithelial Cell ◽  
Complex Lipid ◽  
Small Intestinal ◽  
Lipid Liposomes

Transport and uptake effects of marine complex lipid liposomes in Caco-2 and M cell monolayer models.

Regulation of α1-antitrypsin gene expression in human intestinal epithelial cell line Caco-2 by HNF-1α and HNF-4

1999 ◽  
Vol 276 (5) ◽  
pp. G1181-G1194 ◽  
Author(s):  
Chaobin Hu ◽  
David H. Perlmutter
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Epithelial Cell Line ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cell ◽  
Mobility Shift ◽  
Electrophoretic Mobility Shift Assays ◽  
Enterocyte Differentiation

There is still relatively limited information about mechanisms of gene expression in enterocytes and mechanisms by which gene expression is regulated during enterocyte differentiation. Using the human intestinal epithelial cell line Caco-2, which spontaneously differentiates from a cryptlike to a villouslike enterocyte, we have previously shown that there is a marked increase in transcription of the well-characterized α1-antitrypsin (α1-AT) gene during enterocyte differentiation. In this study we examined the possibility of identifying the cis-acting elements and trans-acting DNA-binding proteins responsible for expression of the α1-AT gene in Caco-2 cells during differentiation. Footprint analysis and electrophoretic mobility shift assays showed that hepatocyte nuclear factor-1α (HNF-1α), HNF-1β, and HNF-4 from nuclear extracts of Caco-2 cells specifically bound to two regions in the proximal promoter of the α1-AT gene. Cotransfection studies showed that HNF-1α and HNF-4 had a synergistic effect on α1-AT gene expression. RNA blot analysis showed that HNF-1α and HNF-4 mRNA levels and electrophoretic mobility shift assays showed that HNF-1α binding activity increase coordinately with α1-AT mRNA levels during differentiation of Caco-2 cells. Finally, overexpression of antisense ribozymes for HNF-1α in Caco-2 cells resulted in a selective decrease in endogenous α1-AT gene expression. Together, these results provide evidence that HNF-1α and HNF-4 play a role in the mechanism by which the α1-AT gene is upregulated during enterocyte differentiation in the model Caco-2 cell system.

scholarly journals Regulation of intracellular Zn homeostasis in two intestinal epithelial cell models at various maturation time points

2015 ◽  
Vol 65 (4) ◽  
pp. 317-328 ◽  
Author(s):  
Eva-Maria Gefeller ◽  
Angelika Bondzio ◽  
Jörg R. Aschenbach ◽  
Holger Martens ◽  
Ralf Einspanier ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
Maturation Time ◽  
Time Points ◽  
Zn Homeostasis

Gene expression study of two widely used pig intestinal epithelial cell lines: IPEC-J2 and IPI-2I

2009 ◽  
Vol 131 (3-4) ◽  
pp. 278-284 ◽  
Author(s):  
Valentina Mariani ◽  
Simona Palermo ◽  
Silvia Fiorentini ◽  
Alessandra Lanubile ◽  
Elisabetta Giuffra
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Cell Lines ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Gene Expression Study ◽  
Expression Study ◽  
Epithelial Cell Lines

scholarly journals Arcobacter butzleri isolates exhibit pathogenic potential in intestinal epithelial cell models

2015 ◽  
Vol 120 (1) ◽  
pp. 218-225 ◽  
Author(s):  
G. Karadas ◽  
R. Bücker ◽  
S. Sharbati ◽  
J.-D. Schulzke ◽  
T. Alter ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
Pathogenic Potential ◽  
Arcobacter Butzleri

The acetylome regulators Hdac1 and Hdac2 differently modulate intestinal epithelial cell dependent homeostatic responses in experimental colitis

2014 ◽  
Vol 306 (7) ◽  
pp. G594-G605 ◽  
Author(s):  
Naomie Turgeon ◽  
Julie Moore Gagné ◽  
Mylène Blais ◽  
Fernand-Pierre Gendron ◽  
François Boudreau ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Intestinal Permeability ◽  
Intestinal Epithelial Cell ◽  
Inflammatory Responses ◽  
Activity Index ◽  
Specific Gene ◽  
Intestinal Epithelial ◽  
Specific Loss ◽  
Deficient Mice

Histone deacetylases (Hdac) remove acetyl groups from proteins, influencing global and specific gene expression. Hdacs control inflammation, as shown by Hdac inhibitor-dependent protection from dextran sulfate sodium (DSS)-induced murine colitis. Although tissue-specific Hdac knockouts show redundant and specific functions, little is known of their intestinal epithelial cell (IEC) role. We have shown previously that dual Hdac1/ Hdac2 IEC-specific loss disrupts cell proliferation and determination, with decreased secretory cell numbers and altered barrier function. We thus investigated how compound Hdac1/ Hdac2 or Hdac2 IEC-specific deficiency alters the inflammatory response. Floxed Hdac1 and Hdac2 and villin-Cre mice were interbred. Compound Hdac1/ Hdac2 IEC-deficient mice showed chronic basal inflammation, with increased basal disease activity index (DAI) and deregulated Reg gene colonic expression. DSS-treated dual Hdac1/ Hdac2 IEC-deficient mice displayed increased DAI, histological score, intestinal permeability, and inflammatory gene expression. In contrast to double knockouts, Hdac2 IEC-specific loss did not affect IEC determination and growth, nor result in chronic inflammation. However, Hdac2 disruption protected against DSS colitis, as shown by decreased DAI, intestinal permeability and caspase-3 cleavage. Hdac2 IEC-specific deficient mice displayed increased expression of IEC gene subsets, such as colonic antimicrobial Reg3b and Reg3g mRNAs, and decreased expression of immune cell function-related genes. Our data show that Hdac1 and Hdac2 are essential IEC homeostasis regulators. IEC-specific Hdac1 and Hdac2 may act as epigenetic sensors and transmitters of environmental cues and regulate IEC-mediated mucosal homeostatic and inflammatory responses. Different levels of IEC Hdac activity may lead to positive or negative outcomes on intestinal homeostasis during inflammation.

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