Iron-related transcriptomic variations in CaCo-2 cells, an in vitro model of intestinal absorptive cells

2006 ◽  
Vol 26 (1) ◽  
pp. 55-67 ◽  
Author(s):  
Céline Chicault ◽  
Bertrand Toutain ◽  
Annabelle Monnier ◽  
Marc Aubry ◽  
Patricia Fergelot ◽  
...  
Keyword(s):  
Gene Expression ◽  
Functional Annotation ◽  
In Vitro Model ◽  
Iron Absorption ◽  
Intracellular Iron ◽  
Absorptive Cells ◽  
Number Of Genes ◽  
Vitro Model ◽  
First Time

Regulation of iron absorption by duodenal enterocytes is essential for the maintenance of homeostasis by preventing iron deficiency or overload. Despite the identification of a number of genes implicated in iron absorption and its regulation, it is likely that further factors remain to be identified. For that purpose, we used a global transcriptomic approach, using the CaCo-2 cell line as an in vitro model of intestinal absorptive cells. Pangenomic screening for variations in gene expression correlating with intracellular iron content allowed us to identify 171 genes. One hundred nine of these genes are clustered into five types of expression profile. This is the first time that most of these genes have been associated with iron metabolism. Functional annotation of these five clusters indicates potential links between the immune response, proteolysis processes, and iron depletion. In contrast, iron overload is associated with cellular metabolism, especially that of lipids and glutathione involving redox function and electron transfer.

scholarly journals A Central Role for the Armadillo Protein Plakoglobin in the Autoimmune Disease Pemphigus Vulgaris

2001 ◽  
Vol 153 (4) ◽  
pp. 823-834 ◽  
Author(s):  
Reto Caldelari ◽  
Alain de Bruin ◽  
Dominique Baumann ◽  
Maja M. Suter ◽  
Christiane Bierkamp ◽  
...  
Keyword(s):  
Steric Hindrance ◽  
In Vitro Model ◽  
Molecular Mechanisms ◽  
Pemphigus Vulgaris ◽  
Cell Types ◽  
Linear Distribution ◽  
Igg Binding ◽  
Vitro Model ◽  
First Time

In pemphigus vulgaris (PV), autoantibody binding to desmoglein (Dsg) 3 induces loss of intercellular adhesion in skin and mucous membranes. Two hypotheses are currently favored to explain the underlying molecular mechanisms: (a) disruption of adhesion through steric hindrance, and (b) interference of desmosomal cadherin-bound antibody with intracellular events, which we speculated to involve plakoglobin. To investigate the second hypothesis we established keratinocyte cultures from plakoglobin knockout (PG−/−) embryos and PG+/+ control mice. Although both cell types exhibited desmosomal cadherin-mediated adhesion during calcium-induced differentiation and bound PV immunoglobin (IgG) at their cell surface, only PG+/+ keratinocytes responded with keratin retraction and loss of adhesion. When full-length plakoglobin was reintroduced into PG−/− cells, responsiveness to PV IgG was restored. Moreover, in these cells like in PG+/+ keratinocytes, PV IgG binding severely affected the linear distribution of plakoglobin at the plasma membrane. Taken together, the establishment of an in vitro model using PG+/+ and PG−/− keratinocytes allowed us (a) to exclude the steric hindrance only hypothesis, and (b) to demonstrate for the first time that plakoglobin plays a central role in PV, a finding that will provide a novel direction for investigations of the molecular mechanisms leading to PV, and on the function of plakoglobin in differentiating keratinocytes.

scholarly journals SPINK1-induced amelioration of impaired autophagy contributes to suppression of trypsinogen activation in a model of acute pancreatitis

2020 ◽  
Author(s):  
Yuxiao Zhao ◽  
Jianlong Jia ◽  
Abdullah Shopit ◽  
Yang Liu ◽  
Jun Wang
Keyword(s):  
Acute Pancreatitis ◽  
In Vitro Model ◽  
Autophagic Flux ◽  
Trypsin Activity ◽  
Autophagy Flux ◽  
Trypsinogen Activation ◽  
Vitro Model ◽  
First Time ◽  
Induced Amelioration

AbstractSPINK1 has been regarded as a reversible trypsinogen inhibitor for the inappropriate activation of trypsin, a key step in the initiation of acute pancreatitis (AP). However, the mechanisms of its action remains largely unclear and controversial. Here, we reported an unexpected effects of SPINK1 on inhibiting trypsinogen activation through the regulation of impaired autophagy in cerulein-stimulated AR42J cells, a well-established in vitro model of acute pancreatitis. Firstly, we found that the impaired autophagic flux was induced and trypsinogen activity enhanced in the above setting. Then, we showed that SPINK1 overexpression could inhibit the level of increased autophagic activity, improving the hindered autophagy flux, and significantly decreased the trypsinogen activity, whereas shRNA-caused downregulation of SPINK1 exacerbated the impairment of autophagic flux and trypsin activity, in the same cerulein-processed cells. More importantly, the trypsinogen activation in this model could be ameliorated by 3-Methyladenine(3-MA), an autophagy inhibitor. Thus, this study revealed, possibly for the first time, that SPINK1 greatly blocked the trypsinogen activation possibly through the modulation of impaired autophagy in cerulein-induced in vitro model of acute pancreatitis.

In vitro model of angiogenesis using a human endothelium-derived permanent cell line: Contributions of induced gene expression, G-proteins, and integrins

1992 ◽  
Vol 153 (3) ◽  
pp. 437-449 ◽  
Author(s):  
Jeffrey Bauer ◽  
Michael Margolis ◽  
Clara Schreiner ◽  
Cora-Jean Edgell ◽  
Jane Azizkhan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
G Proteins ◽  
In Vitro Model ◽  
Permanent Cell Line ◽  
Permanent Cell ◽  
Vitro Model ◽  
Human Endothelium

Establishment and characterization of a piscean PCF cell line for toxicity and gene expression studies as in vitro model

2014 ◽  
Vol 46 (3) ◽  
pp. 206-212 ◽  
Author(s):  
M. Goswami ◽  
B.S. Sharma ◽  
Kamalendra Yadav ◽  
S.N. Bahuguna ◽  
W.S. Lakra
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
In Vitro Model ◽  
Expression Studies ◽  
Gene Expression Studies ◽  
Vitro Model
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