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At least 145 records · Page 8Linked to original sources
PubMed1995

Effect of enprostil and cimetidine on ethanol-induced damage to intestinal epithelial cell lines IRD 98 and IEC 17.

In addition to their inhibitory action on gastric acid secretion, prostaglandins may exert part of their protective effect on the gastrointestinal mucosa by specifically maintaining the cellular integrity of the intestinal epithelium. This in vitro study investigated the cytoprotective effect conferred on intestinal epithelial cell lines IRD 98 and IEC 17 against ethanol injury by the synthetic prostaglandin enprostil and compared effects with those of the histamine H2-receptor blocker cimetidine. Exposure to 3% ethanol (652 mM) reduced cell viability and increased the cAMP and membrane fluidity of both cell lines. Our results demonstrate that: (i) enprostil exerts a significant cytoprotective effect against damage by ethanol; (ii) cimetidine has no cytoprotective effect; (iii) IRD 98 cells are more sensitive to enprostil than IEC 17 cells.

Animals↗
PubMed1995

Effects of lactoferrin and its peptides on proliferation of rat intestinal epithelial cell line, IEC-18, in the presence of epidermal growth factor.

The cell growth-stimulating activity of lactoferrin (LF) in combination with epidermal growth factor (EGF) was evaluated by using a rat intestinal epithelial cell line, IEC-18. LF was found to be more effective than EGF for inducing an increase in cell numbers when cultured for over 6 days using a medium containing 0.2% fetal calf serum (FCS), although the 3H-thymidine incorporation-stimulating activity of EGF was more potent than that of LF. A synergistic effect of LF and EGF was observed in both cell proliferation and DNA synthesis assays. The increase in cell numbers when stimulated with LF plus EGF corresponded to about 5 times that of the control. Iron was not required for manifestation of these effects of LF. On the other hand, iron-saturated transferrin (TF) had cell-growth-stimulating activity, but iron-free TF did not, either in the presence or absence of EGF. These results indicate that LF induces cell proliferation by a mechanism distinct from that of TF. A pepsin-generated hydrolysate of LF (LFH) had an activity similar to that of undigested LF, and a peptide with cell-growth-stimulating activity from bovine LFH was isolated by monitoring its effects in combination with EGF on DNA synthesis in IEC-18 cells. Sequence analysis indicated that the peptide has the structure Ala-Glu-Ile-Tyr-Gly-Thr-Lys-Glu-Ser-Pro-Gln-Thr-His-Tyr-Tyr, corresponding to residues 79-93 of bovine LF.

Amino Acid Sequence↗
PubMed1997

Cytotoxicity of cholestane 3 beta,5 alpha,6 beta-triol on cultured intestinal epithelial crypt cells (IEC-6).

The effects of cholestane 3 beta,5 alpha,6 beta-triol on intestinal epithelial crypt cells were investigated using the IEC-6 cell line. Cholestane 3 beta,5 alpha,6 beta-triol decreased SH groups (glutathione and protein SH) in the cell, and showed cytotoxicity in a time-dependent manner. Although the concentration of cholestane 3 beta,5 alpha,6 beta-triol used in this study (100 microM) was very high compared with that in plasma of experimental animals, cholestane 3 beta,5 alpha,6 beta-triol did not show any cytotoxicity on IEC-6 cells without fetal calf serum (FCS). The level of cytotoxicity was dependent upon the concentration of FCS in the culture medium. Unknown components in FSC (not VLDL or LDL) were suggested to be associated with the cytotoxicity of cholestane 3 beta,5 alpha,6 beta-triol. Moreover, the fact that even heat-treated FCS (100 degrees C for 30 min) still mediated the cytotoxicity suggested the participation of non-protein components.

Animals↗
PubMed2005

Ephrin-B reverse signaling induces expression of wound healing associated genes in IEC-6 intestinal epithelial cells.

AIM: Eph receptors and ephrin ligands play a pivotal role in development and tissue maintenance. Since previous data have indicated an involvement of ephrin-B2 in epithelial healing, we investigated the gene expression and downstream signaling pathways induced by ephrin-B mediated cell-cell signaling in intestinal epithelial cells. METHODS: Upon stimulation of ephrin-B pathways in IEC-6 cells with recombinant rat EphB1-Fc, gene expression was analyzed by Affymetrix(R) rat genome 230 high density arrays at different time points. Differentially expressed genes were confirmed by real-time RT-PCR. In addition, MAP kinase pathways and focal adhesion kinase (FAK) activation downstream of ephrin-B were investigated by immunoblotting and fluorescence microscopy. RESULTS: Stimulation of the ephrin-B reverse signaling pathway in IEC-6 cells induces predominant expression of genes known to be involved into wound healing/cell migration, antiapoptotic pathways, host defense and inflammation. Cox-2, c-Fos, Egr-1, Egr-2, and MCP-1 were found among the most significantly regulated genes. Furthermore, we show that the expression of repair-related genes is also accompanied by activation of the ERK1/2 MAP kinase pathway and FAK, two key regulators of epithelial restitution. CONCLUSION: Stimulation of the ephrin-B reverse signaling pathway induces a phenotype characterized by upregulation of repair-related genes, which may partially be mediated by ERK1/2 pathways.

Animals↗
PubMed2000

Distinct mechanisms of transport of ascorbic acid and dehydroascorbic acid in intestinal epithelial cells (IEC-6).

Ascorbic acid (AsA) is an essential nutrient for humans as they lack its biosynthesizing key enzyme. Its absorption mechanism in small intestinal epithelial cells still remains to be resolved. In this study, the transport mechanisms functioning on the uptake of AsA and its oxidized form, dehydroascorbic acid (DHA), were investigated using rat small intestinal epithelial cell line IEC-6. Both AsA and DHA were accumulated in the cells in time- and concentration-dependent manners, but their absorption kinetics were apparently different. The saturability of AsA uptake was shown at a considerably lower concentration in IEC-6 cells as well as other mammalian cells, indicating that this absorption was mediated by a specific transporting carrier. The absorption efficiency of AsA was about 1/5-1/10 that of DHA at the same concentration range and, moreover, the uptake of DHA was almost comparable to that of 2-deoxy-D-glucose, an alternative of glucose. The uptake of AsA was diminished by the removal of sodium ion, but not by the addition of glucose, whereas that of DHA was sodium ion-independent and effectively inhibited by glucose. In addition, phlorizin and cytochalasin B, which are blockers of glucose transporters, interfered the uptake of DHA more efficiently than that of AsA. These results indicate that there are at least two distinct transport systems of vitamin C in rat small intestinal epithelial cells; AsA is transported by a specific transporter and DHA is mainly transported by glucose transporter(s).

Animals↗
PubMed1993

Rat intestinal epithelial cell line IEC-6 is activated by recombinant interferon-gamma to inhibit replication of the coccidian Toxoplasma gondii.

Toxoplasma gondii tachyzoites invaded and replicated in cultured rat small intestine cells of the line IEC-6. Treatment of rat small intestine cells with murine recombinant interferon-gamma resulted in a dose-dependent inhibition of intracellular T. gondii replication. This could be of relevance as a first line defense against Toxoplasma infection.

Animals↗
PubMed1997

Sodium-dependent and -independent transport of L-glutamate in the rat intestinal crypt-like cell line IEC-17.

Mechanisms of L-glutamate transport in intestinal crypts were investigated using the rat intestinal crypt-like cell line IEC-17. Kinetic analysis and competition experiments run in the presence or in the absence of extracellular sodium indicate that L-glutamate uptake occurs through three different transport components: (1) a high affinity Na+-independent component also carrying cystine, similar to system x(c)-; (2) a high affinity Na+-dependent component inhibited by D- and L-aspartate corresponding to the ubiquitous system X(A,G)-; and (3) a low affinity Na+-dependent system resembling the neutral amino acid transport system ASC. The simultaneous presence of these three components suggest that crypt cells are ready to face potential high variations of L-glutamate concentration in the intestinal villus environment.

Animals↗
PubMed1999

TNFalpha-induced IEC-6 cell apoptosis requires activation of ICE caspases whereas complete inhibition of the caspase cascade leads to necrotic cell death.

Tumor necrosis factor (TNF)alpha is considered to play a key pathogenetic role in inflammatory bowel diseases. In this study we analyzed the mechanisms by which TNFalpha induces intestinal epithelial cell apoptosis. TNFalpha alone, and more potently in combination with IFNgamma, induced a high degree of IEC-6 cell apoptosis. This effect was more than 100-fold stronger if both of the TNF-R were stimulated, compared to stimulation of the p55-TNF-R alone, indicating an important apoptosis enhancing effect of the p75-TNF-R. TNFalpha-induced apoptosis required activation of ICE caspases and was completely abolished by its inhibitor, zVAD-fmk. Specific inhibition of caspase-3 with zDEVD-fmk did not alter the effect of TNFalpha. Western blot analyses confirmed that caspase-3 was not activated in response to TNFalpha. In the presence of complete inhibition of the caspase cascade with zVAD-fmk (>/=50 microM), TNFalpha induced cell necrosis rather than apoptosis. Our data reveal that TNFalpha can trigger enterocyte cell death via apoptosis or necrosis, depending upon the activation or blockade of specific caspases.

Amino Acid Chloromethyl Ketones↗
PubMed1996

Regulation of CCAAT/enhancer binding protein isoforms by serum and glucocorticoids in the rat intestinal epithelial crypt cell line IEC-6.

Members of the CCAAT/enhancer binding protein (C/EBP) gene family are expressed in murine intestine. However, little is known about their regulation in intestinal epithelial cells. In an attempt to determine regulatory mechanisms involved in their expression, we examined C/EBP alpha, beta, and delta isoform expression in response to serum and glucocorticoids in the rat intestinal epithelial crypt-derived cell line IEC-6, by Northern blot, transcription run-on assays, indirect immunofluorescence, Western blot, and electrophoretic mobility shift assays. Serum leads to rapid and transient increases in C/EBP alpha and beta mRNA and protein levels by posttranscriptional regulatory mechanisms, without affecting transcriptional initiation. However, C/EBP-specific DNA binding capacity is not affected by serum. Whereas C/EBP alpha expression is not regulated by glucocorticoids, C/EBP beta and delta mRNA and protein levels are rapidly induced. These inductions result from both increased transcription rates and posttranscriptional regulatory mechanisms as well. Moreover, C/EBP beta and delta containing DNA binding complexes are increased by glucocorticoids as determined by supershift assays, in contrast to C/EBP alpha containing complexes. Immunofluorescence studies show cytoplasmic and nuclear localization for C/EBP alpha, in contrast to a restricted nuclear localization for both C/EBP beta and C/EBP delta. These results confirm C/EBP isoforms expression in intestinal epithelial cells. Differential regulation by serum and glucocorticoids as well as different localization of three C/EBP isoforms suggest a role for this class of transcription factors in the control of gene expression in intestinal epithelial cells.

Animals↗
PubMed2004

Differences in the uptake of iron from Fe(II) ascorbate and Fe(III) citrate by IEC-6 cells and the involvement of ferroportin/IREG-1/MTP-1/SLC40A1.

Dietary iron is present in the intestine as Fe(II) and Fe(III). Since enterocytes take up Fe(II) by the divalent metal transporter (DMT1), Fe(III) must be reduced. Whether other Fe(III) transport processes are present is unknown. Release of iron from the enterocyte into the plasma involves the iron-regulated transporter-1/metal transporter protein-1 (IREG-1/MTP-1, ferroportin) but ferroportin is also found on the apical membrane. We compared the uptake of iron from Fe(II):ascorbate and Fe(III):citrate using the rat intestinal enterocyte cell line-6 (IEC-6), in the presence of ferrous chelators, a blocking antibody to ferroportin, at different pH and during the over-expression of DMT1. Firstly, surface ferrireduction was absent. Secondly, blocking ferroportin partly and totally reduced Fe(II) and Fe(III) uptake, respectively. Thirdly, optimal Fe(II) uptake occurred at pH 5.5 but Fe(III) uptake was unaffected by pH and, fourthly, over-expression of DMT1 increased uptake of Fe(II) and Fe(III). This indicates that an increased extracellular H+ concentration facilitates DMT1-mediated Fe(II) uptake at the cell membrane. However, since Fe(III) uptake required DMT1, but not cell surface ferrireduction, and was independent of variations in extracellular pH, it appears that Fe(III) is internalised before ferrireduction and transport by DMT1. Ferroportin may function as a modulator of DMT1 activity and play a role in Fe(III) uptake, possibly by affecting the number or affinity of citrate binding sites.

Animals↗
PubMed1991

Putrescine uptake and release by a normal rat small intestine crypt cell line, IEC-6.

IEC-6 cells were cultured on permeable filter inserts with separate access to the apical and basolateral sides. [3H]Putrescine uptake favored the apical side and its release (in Earle's balanced salt solution containing 0.1% bovine serum albumin) was six times greater in the apical-to-basolateral than in the basolateral-to-apical direction. Release in DMEM did not show this preference. The uptake of [3H]putrescine was stimulated approximately 1.3 times the basal level by 10 mM asparagine (ASN) or 5% dialyzed fetal bovine serum whether the [3H]putrescine was added at a concentration of 1 or 100 nM. The increased uptake was maintained for up to 6 h. When [3H]putrescine was removed after 4 h of uptake, the cells continued to release it into the medium on both sides for up to 4 h. Stimulated cells released only 50% as much as unstimulated cells. Unlabeled putrescine reduced the uptake of [3H]putrescine with an IC50 of 1.81 x 10(-6) M (r = 0.9476) and 1.02 x 10(-6) M (r = 0.9967) for unstimulated and ASN-stimulated cells, respectively. When the intracellular putrescine was reduced by difluoromethylornithine, the uptake of [3H]-putrescine was not changed, but its release was inhibited. Sodium was not required for [3H]putrescine uptake or release. Although the stimulated cells attained intracellular levels of [3H]putrescine which, if expressed as concentration based on cell volume, were up to 500 times the original extracellular concentration, a true concentration gradient could not be proven because 85% of the [3H]putrescine was probably bound to polyanions as shown by butanol extraction.

Animals↗
PubMed1995

Identification of atypical (non-AT1, non-AT2) angiotensin binding sites with high affinity for angiotensin I on IEC-18 rat intestinal epithelial cells.

Specific high-affinity (Kd = 3.4 nM) binding sites for 125I-labelled angiotensin I ([125I]Ang I) were identified on an epithelial cell line (IEC-18) derived from the rat small intestine. The sites, which also have high affinity for Ang II, are insensitive to both AT1- and AT2-specific angiotensin receptor antagonists. The rank order of potency with which various angiotensin peptides inhibited [125I]Ang I binding to the cells (Ang I > or = Ang II > Ang(1-7) > [Sar1,Ile8]-Ang II > Ang(3-8) > Ang III) also distinguishes these sites from AT1 and AT2 angiotensin receptors.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1991

Transforming growth factor-beta enhances secretory component and major histocompatibility complex class I antigen expression on rat IEC-6 intestinal epithelial cells.

Transforming growth factor-beta (TGF-beta) has been implicated as having a role in inflammatory responses by inducing cellular infiltration and the release of inflammatory cytokines. In this study, the IEC-6 rat intestinal epithelial cell line was used as a model to assess the effect of TGF-beta 1 on the expression of various plasma membrane determinants. TGF-beta 1 induced a dose-dependent increase in the percentage of cells expressing surface secretory component (SC) and class I major histocompatibility (MHC) antigens. However, the expression of class II MHC was unaffected. In contrast, epidermal growth factor had no effect on any of the surface proteins studied. The TGF-beta 1-enhanced expression of SC was accompanied by an enhanced binding of polymeric, but not monomeric, immunoglobulin A (IgA). Preincubation of the TGF-beta 1-treated cells with an anti-human beta-galactosyltransferase (beta-GT) antiserum did not block the binding of the anti-SC antibody, indicating that the TGF-beta-induced increase in SC staining was due to SC expression and not the polymeric immunoglobulin-binding enzyme, beta-GT. These results indicate that TGF-beta 1 may be important in immune functions involving intestinal epithelial cells by enhancing the expression of surface class I MHC antigens and SC, a protein responsible for the transport of polymeric IgA into the intestinal lumen.

Animals↗
PubMed2000

Soft-testing of industrial control systems programmed in IEC 1131-3 languages.

This paper presents a technique and the means for testing PLC-based control software outside the actual plant environment with the purpose of increasing the confidence level on the compliance of the software to functional and temporal requirements. The need to obtain a high confidence level on the correct software operation arises from the fact that in most of the cases it is quite dangerous and expensive to test unproved PLC operation by linking it with the actual facilities that it is going to control. The proposed technique relies on a combined simulation of the controlled plant and the PLC system and an analysis of the plant responses. The PLC system simulation imitates the way software is executed on a PLC that is programmed in the languages of the IEC1131-3 standard. It is based on the programming model of the IEC standard and analytical formulae for estimating the program runtime. The simulation of the plant is based on a discrete convolution model that is solved at the same rate with the rate determined by the control algorithms. A tool realizing these concepts has been developed and its use in testing the control software of three critical outputs of a distillation column is demonstrated.

Computer Simulation↗
PubMed1998

Calphostin C induces expression of amphiregulin mRNA via reactive oxygen species in IEC-6 cells.

Calphostin C, a secondary metabolite of the fungus Cladosporium cladosporioides, is generally used as a specific inhibitor of protein kinase C. It is known that 12-O-tetradecanoyl-13-phorbol acetate (TPA), a protein kinase C activator, induces expression of mRNA for amphiregulin (AR), a member of EGF-related polypeptides, in mammalian epithelial cells. In this work, we determined the effect of calphostin C on AR mRNA expression in IEC-6 cells, a rat intestinal epithelial cell line, and unexpectedly found that this compound enhanced the TPA-induced expression of AR mRNA. Moreover, calphostin C alone induced expression of AR mRNA in a light-dependent manner, and this effect was abrogated by pretreatment with N-acetylcysteine. These results suggest that calphostin C can upregulate expression of AR mRNA via reactive oxygen species.

Acetylcysteine↗
PubMed2002

N-3 and n-6 fatty acids stimulate restitution by independent mechanisms in the IEC-6 model of intestinal wound healing.

We have shown that intestinal epithelial restitution is stimulated by n-3 and n-6 fatty acids. The current studies were undertaken to elucidate the mechanistic pathway(s) involved in this fatty acid modulation of restitution. Inhibition of phospholipase A(2) and eicosanoid synthesis and its effect on fatty acid stimulation of cellular migration in confluent, wounded IEC-6 monolayers was examined. The production of prostaglandin E(2) and transforming growth factor beta(1) were also measured in fatty acid supplemented cultures. Inhibition of phospholipase A(2) attenuated the effect of fatty acid stimulation of restitution in both n-3 and n-6 supplemented cultures. The lipoxygenase inhibitor, nordihydorguaretic acid (2 &mgr;mol/L), had no effect on stimulation of migration by fatty acids. The cyclooxygenase inhibitor piroxicam (5 &mgr;mol/L) and cyclooxygenase-2 specific inhibitors dexamethasone (2 &mgr;mol/L) and NS-398 (10 &mgr;mol/L) all attenuated the fatty acid stimulation of migration by n-6 fatty acids but had no effect on n-3 stimulated restitution. Prostaglandin E(2) production in n-6 supplemented cultures was significantly greater than in control and n-3 supplemented cultures and was partially inhibited by dexamethasone and NS-398. Latent transforming growth factor beta(1) production in n-3 supplemented cultures was significantly higher than baseline and n-6 supplemented cultures. Docosapentaenoic acid supplementation significantly enhanced the restitution process and NS-398 treatment had no effect on this stimulation of cellular migration. The liberation of fatty acid from the sn-2 position of phospholipid appears to be necessary for both n-3 and n-6 fatty acid stimulation of restitution. N-6 fatty acid modulation of restitution appears to be mediated through the production of eicosanoid products, however, prostaglandin E(2) does not appear to be the sole prostanoid involved. N-3 supplementation elevates the production of latent transforming growth factor beta(1) and may be responsible for n-3 mediated stimulation of restitution. These results further emphasize that n-3 and n-6 fatty acids convey their effects through unique pathways.

Journal Article↗
PubMed2000

The IEC star-mode fusion neutron source for NAA--status and next-step designs

Based on research at the University of Illinois, a commercial neutron source has been developed by Daimler Chrysler Aerospace using a small grided-type Inertial Electrostatic Confinement (IEC) plasma device (Miley and Sved, 1997) This device employs a unique "Star-Mode" deuterium plasma discharge to create ion-beam driven fusion reactions in a plasma target (Miley et al., 1997a, 1997b, 1997c; Miley, 1999). As such, it represents the first commercial application of a confined fusing plasma. The Star-Mode discharge is an essential feature of this device since it minimizes ion-grid collisions and also allows tight beam focussing.

Journal Article↗
PubMed2001

Phorbol ester treatment increases paracellular permeability across IEC-18 gastrointestinal epithelium in vitro.

The phorbol ester, TPA, transiently increases the transepithelial permeability across the gastrointestinal epithelium formed by IEC-18. There was a significant decrease in transepithelial resistance (R(T)) between 0 and 1.5 hr, accompanied by increased flux of polyethylene glycol (4000 MW), suggesting that the increase was across the tight junction. By 2 hr, the decrease in R(T) reversed and maintained control level. The transepithelial permeability increase was prevented by coincubation with the protein kinase C (PKC) inhibitor bisindolylmaleimide. There was a rapid (within 15 min) translocation of PKC-alpha from the cytosolic to the "membrane-associated" compartment, followed by a down-regulation that was detectable within 60 min of TPA treatment. The down-regulation of PKC-alpha from the membrane was prevented by either calpain inhibitor I or MG-132 and resulted in a sustained permeability increase. The permeability changes were not accompanied by significant effects on the amount or localization of the tight junctional proteins, occludin and ZO-1. However, occludin did show a reversible increase in phosphorylation with TPA treatment. Together these data support a role for PKC-alpha-mediated regulation of barrier permeability in an in vitro model of small intestinal epithelium, perhaps through modulation of the phosphorylation state of the tight junctional protein, occludin.

Animals↗