scholarly journals Fucosylation and protein glycosylation create functional receptors for cholera toxin

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Amberlyn M Wands ◽  
Akiko Fujita ◽  
Janet E McCombs ◽  
Jakob Cervin ◽  
Benjamin Dedic ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Surface ◽  
Cholera Toxin ◽  
Protein Glycosylation ◽  
Host Cells ◽  
Epithelial Cell Line ◽  
Colonic Epithelial Cell ◽  
Surface Receptors ◽  
Intestinal Epithelia ◽  
Epithelial Cell Lines

Cholera toxin (CT) enters and intoxicates host cells after binding cell surface receptors using its B subunit (CTB). The ganglioside (glycolipid) GM1 is thought to be the sole CT receptor; however, the mechanism by which CTB binding to GM1 mediates internalization of CT remains enigmatic. Here we report that CTB binds cell surface glycoproteins. Relative contributions of gangliosides and glycoproteins to CTB binding depend on cell type, and CTB binds primarily to glycoproteins in colonic epithelial cell lines. Using a metabolically incorporated photocrosslinking sugar, we identified one CTB-binding glycoprotein and demonstrated that the glycan portion of the molecule, not the protein, provides the CTB interaction motif. We further show that fucosylated structures promote CTB entry into a colonic epithelial cell line and subsequent host cell intoxication. CTB-binding fucosylated glycoproteins are present in normal human intestinal epithelia and could play a role in cholera.

scholarly journals Bilirubin Attenuates ER Stress-Mediated Inflammation, Escalates Apoptosis and Reduces Proliferation in the LS174T Colonic Epithelial Cell Line

2019 ◽  
Vol 16 (1) ◽  
pp. 135-144 ◽  
Author(s):  
Rohit Gundamaraju ◽  
Ravichandra Vemuri ◽  
Wai Chin Chong ◽  
Andrew Cameron Bulmer ◽  
Rajaraman Eri
Keyword(s):  
Epithelial Cell ◽  
Er Stress ◽  
Cell Line ◽  
Epithelial Cell Line ◽  
Colonic Epithelial Cell ◽  
Colonic Epithelial Cell Line

Vasoactive intestinal peptide stimulates protein phosphorylation in a colonic epithelial cell line

1987 ◽  
Vol 253 (3) ◽  
pp. G420-G424 ◽  
Author(s):  
J. A. Cohn
Keyword(s):  
Epithelial Cell ◽  
Ion Transport ◽  
Protein Phosphorylation ◽  
Cell Line ◽  
Vasoactive Intestinal Peptide ◽  
Epithelial Cell Line ◽  
Colonic Epithelial Cell ◽  
Ussing Chambers ◽  
Colonic Epithelial Cell Line ◽  
Stimulation Of

The T84 colonic epithelial cell line was used to examine protein phosphorylation during neurohumoral stimulation of ion transport. T84 cell monolayers grown on collagen-coated filters were mounted in Ussing chambers to measure ion transport stimulated by vasoactive intestinal peptide. Maximal stimulation of active secretion occurred after 8-10 min of stimulation. Protein phosphorylation events accompanying stimulated secretion were detected using two-dimensional gel electrophoresis to resolve phosphoproteins from monolayers previously labeled using 32Pi. Within 8 min of exposure to vasoactive intestinal peptide, several phosphorylation events were detected, including a two- to fivefold increase in 32P incorporation into four soluble proteins with apparent molecular weights of 17,000, 18,000, 23,000, and 37,000. The same phosphorylation response occurs in monolayers stimulated by dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP), suggesting that cAMP mediates these intracellular events. This study indicates that changes in protein phosphorylation accompany the secretory action of vasoactive intestinal peptide and suggests that T84 cells offer a useful model for studying the possibility that such phosphorylation events regulate enterocyte ion transport.

MicroRNA-212 targets SIRT2 to influence lipogenesis in bovine mammary epithelial cell line

2020 ◽  
Vol 87 (2) ◽  
pp. 232-238
Author(s):  
Xubin Lu ◽  
Hailei Xia ◽  
Jingyi Jiang ◽  
Xin Xu ◽  
Mingxun Li ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Lines ◽  
Mammary Epithelial Cell ◽  
Regulatory Element ◽  
Fatty Acid Synthetase ◽  
Mammary Epithelial ◽  
Epithelial Cell Line ◽  
Peroxisome Proliferator ◽  
Epithelial Cell Lines ◽  
Verification Techniques

AbstractIn this research paper we filter and verify miRNAs which may target silent information regulator homolog 2 (SIRT2) gene and then describe the mechanism whereby miRNA-212 might regulate lipogenic genes in mammary epithelial cell lines via targeting SIRT2. Bioinformatics analysis revealed that the bovine SIRT2 gene is regulated by three miRNAs: miR-212, miR-375 and miR-655. The three miRNAs were verified and screened by qRT-PCR, western blot, and luciferase multiplex verification techniques and only miR-212 was shown to have a targeting relationship with SIRT2. The results of co-transfecting miR-212 and silencing RNA (siRNA) showed that by targeting SIRT2, miR-212 can regulate the expression of fatty acid synthetase (FASN) and sterol regulatory element binding factor 1 (SREBP1) but not peroxisome proliferator-activated receptor gamma (PPARγ). Measurement of triglyceride (TAG) content showed that miR-212 increased the fat content of mammary epithelial cell lines. The study indicates that miR-212 could target and inhibit the expression of the SIRT2 gene to promote lipogenesis in mammary epithelial cell lines.

scholarly journals A redox-based mechanism for induction of interleukin-1 production by nitric oxide in a human colonic epithelial cell line (HT29-Cl.16E)

1996 ◽  
Vol 313 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Geneviève VALLETTE ◽  
Anne JARRY ◽  
Jean-Eric BRANKA ◽  
Christian L. LABOISSE
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cell ◽  
Cell Line ◽  
Interleukin 1 ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Colonic Epithelial Cell ◽  
Colonic Epithelial Cell Line ◽  
Dose Dependent ◽  
Human Colonic Epithelial Cell

We evaluated the effects of two NO donors, sodium nitroprusside (SNP) and 3-morpholino-sydnonimine (SIN-1), characterized by alternative redox states, i.e. nitrosonium ion (NO+) and nitric oxide (NO•) respectively, on intracellular interleukin-1 (IL-1) production, by a human colonic epithelial cell line (HT29-Cl.16E). SNP was able to induce intracellular IL-1α production up to 10 h incubation, in a dose-dependent manner. Several experiments provide evidence that the NO+ redox form, and not the free radical NO•, is implicated in the IL-1α production: (i) SIN-1, devoid of any NO+ character, led to a very weak IL-1 production as compared with SNP; (ii) the reductive action of a thiol such as cysteine on NO+ led to a dose-dependent increase in NO• concentration, measured as NO2-/NO3- accumulation, and to a large decrease in IL-1 production. Dibutyryl cGMP had no effect on IL-1 production, this finding supporting the concept that a cGMP-independent pathway is involved in the intracellular signalling of NO+. Together these results point out that NO, depending on its redox form, is able to modulate IL-1 production in cultured colonic epithelial cells.

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