scholarly journals Polyamines inhibit the assembly of stress granules in normal intestinal epithelial cells regulating apoptosis

2012 ◽  
Vol 303 (1) ◽  
pp. C102-C111 ◽  
Author(s):  
Tongtong Zou ◽  
Jaladanki N. Rao ◽  
Lan Liu ◽  
Lan Xiao ◽  
Yu-Hong Cui ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Ornithine Decarboxylase ◽  
Intestinal Epithelial Cells ◽  
Stress Granules ◽  
Initiation Factor ◽  
Intestinal Epithelial ◽  
Eukaryotic Initiation Factor ◽  
Related Protein ◽  
Induced Apoptosis ◽  
Factor Α

Polyamines regulate multiple signaling pathways and are implicated in many aspects of cellular functions, but the exact molecular processes governed by polyamines remain largely unknown. In response to environmental stress, repression of translation is associated with the assembly of stress granules (SGs) that contain a fraction of arrested mRNAs and are thought to function as mRNA storage. Here we show that polyamines modulate the assembly of SGs in normal intestinal epithelial cells (IECs) and that induced SGs following polyamine depletion are implicated in the protection of IECs against apoptosis. Increasing the levels of cellular polyamines by ectopic overexpression of the ornithine decarboxylase gene decreased cytoplasmic levels of SG-signature constituent proteins eukaryotic initiation factor 3b and T-cell intracellular antigen-1 (TIA-1)-related protein and repressed the assembly of SGs induced by exposure to arsenite-induced oxidative stress. In contrast, depletion of cellular polyamines by inhibiting ornithine decarboxylase with α-difluoromethylornithine increased cytoplasmic eukaryotic initiation factor 3b and TIA-1 related protein abundance and enhanced arsenite-induced SG assembly. Polyamine-deficient cells also exhibited an increase in resistance to tumor necrosis factor-α/cycloheximide-induced apoptosis, which was prevented by inhibiting SG formation with silencing SG resident proteins Sort1 and TIA-1. These results indicate that the elevation of cellular polyamines represses the assembly of SGs in normal IECs and that increased SGs in polyamine-deficient cells are crucial for increased resistance to apoptosis.

Actin related protein 3 (ARP3) promotes apoptosis of intestinal epithelial cells in ulcerative colitis

2019 ◽  
Vol 215 (2) ◽  
pp. 235-242
Author(s):  
Shi-Qing Zhang ◽  
Wen-Kai Ni ◽  
Ming-Bing Xiao ◽  
Feng Jiang ◽  
Cui-hua Lu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Related Protein

Sequential and rapid activation of select caspases during apoptosis of normal intestinal epithelial cells

1998 ◽  
Vol 274 (6) ◽  
pp. G1117-G1124 ◽  
Author(s):  
Johannes Grossmann ◽  
Susanne Mohr ◽  
Eduardo G. Lapetina ◽  
Claudio Fiocchi ◽  
Alan D. Levine
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cysteine Proteases ◽  
Intestinal Epithelial ◽  
Caspase Activation ◽  
High Turnover ◽  
Sequential Activation ◽  
Caspase 6 ◽  
Caspase Substrate ◽  
Induced Apoptosis

Detachment-induced cell death (DICD) is considered to be one of the means by which intestinal epithelial cells (IEC) die of apoptosis as they reach the lumen and are shed. Caspases, a family of cysteine proteases, play a central role in initiating, amplifying, and executing apoptosis; however, the pattern of caspase activation in response to distinct apoptotic stimuli remains unknown. We investigated the kinetics of caspase activation during DICD in freshly isolated human IEC. DNA fragmentation is observed 90 min after detachment and is preceded by the sequential activation of preformed members of the CPP32 family of caspases. Activation of caspase 6 and cleavage of the endogenous caspase substrate poly(ADP-ribose) polymerase (EC 2.4.2.30 ) are detected within 15 min of detachment, 30–45 min before caspase 3 activation. Caspase 1 and caspase 10 are present as proenzymes, yet they remain inactive in response to this trigger of apoptosis. Human IEC are primed to rapidly undergo detachment-induced apoptosis involving the selective and sequential activation of preformed caspases. This study may enhance our understanding of physiological events occurring as IEC are shed. Their rapid apoptotic response to detachment may facilitate the high turnover of cells and ensure homeostasis in the intestinal epithelium.

Effects of Stearic Acid on Proliferation, Differentiation, Apoptosis, and Autophagy in Porcine Intestinal Epithelial Cells

2020 ◽  
Vol 20 (2) ◽  
pp. 157-166
Author(s):  
Yuan Yang ◽  
Jin Huang ◽  
Jianzhong Li ◽  
Huansheng Yang ◽  
Yulong Yin
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cells ◽  
Stearic Acid ◽  
Er Stress ◽  
Intestinal Epithelial Cells ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
High Concentrations ◽  
Induced Apoptosis ◽  
Dose Dependent

Background: Stearic acid (SA), a saturated long-chain fatty acid consisting of 18 carbon atoms, is widely found in feed ingredients, such as corn, soybeans, and wheat. However, the roles of SA in the renewal of intestinal epithelial cells remain unclear. Methods and Results: In the present study, we found that 0.01-0.1 mM SA promoted IPEC-J2 cell differentiation and did not affect IPEC-J2 cell viability. In addition, the results showed that the viability of IPEC-J2 cells was inhibited by SA in a time- and dose-dependent manner at high concentrations. Flow cytometry and western blot analysis suggested that SA induced apoptosis, autophagy and ER stress in cells. In addition, the amounts of triglyceride were significantly increased upon challenge with SA. Moreover, the decrease in the viability of cells induced by SA could be attenuated by 4-PBA, an inhibitor of ER stress. Conclusion: In summary, SA accelerated IPEC-J2 cell differentiation at 0.01-0.1 mM. Furthermore, SA induced IPEC-J2 cell apoptosis and autophagy by causing ER stress.

scholarly journals Regulation of NF-κB responses by epigenetic suppression of IκBα expression in HCT116 intestinal epithelial cells

2010 ◽  
Vol 299 (1) ◽  
pp. G96-G105 ◽  
Author(s):  
Angela O'Gorman ◽  
Amy Colleran ◽  
Aideen Ryan ◽  
Jelena Mann ◽  
Laurence John Egan
Keyword(s):  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Epithelial Cells ◽  
Gene Promoter ◽  
Intestinal Epithelial ◽  
Epigenetic Factors ◽  
Factor Α ◽  
Necrosis Factor ◽  
Hct116 Cells

Intestinal epithelial cells play critical roles in regulating mucosal immunity. Since epigenetic factors such as DNA methylation and histone modifications are implicated in aging, carcinogenesis, and immunity, we set out to assess any role for epigenetic factors in the regulation of intestinal epithelial cell immune responses. Experiments were conducted using the HCT116 cell line, and a subclone was genetically engineered to lack DNA methyltransferases (DNMT). The induction of the chemokine interleukin-8 and the antiapoptotic protein cFLIP by tumor necrosis factor-α were markedly less in HCT116 cells lacking DNMT than in parental cells. These effects were accompanied by lower monocyte chemotaxis and higher caspase signaling in HCT116 cells lacking DNMT than parental cells. Tumor necrosis factor-α-induced NF-κB activation was blocked and IκBα expression was higher in HCT116 cells lacking DNMT than in parental cells. A CpG island in the IκBα gene promoter region was found to contain variable levels of methylation in parental HCT116 cells. Chromatin immunoprecipitation analysis of histone proteins bound to the IκBα gene promoter revealed that higher levels of IκBα expression in HCT116 cells lacking DNMT compared with parental cells were accompanied by more chromatin marks permissive to gene transcription. These findings show that epigenetic factors influence the NF-κB system in intestinal epithelial cells, resulting in a previously unrecognized mechanism of innate immune regulation.

Modular effects of estradiol on ethanol-induced apoptosis in human intestinal epithelial cells

2005 ◽  
Vol 40 (3) ◽  
pp. 326-335 ◽  
Author(s):  
Kiyoko Asai ◽  
Wim A. Buurman ◽  
Chris P. M. Reutelingsperger ◽  
Bert Schutte ◽  
Michio Kaminishi
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Induced Apoptosis
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