scholarly journals Endothelin-3 stimulates survival of goblet cells in organotypic cultures of fetal human colonic epithelium

2008 ◽  
Vol 295 (6) ◽  
pp. G1182-G1189 ◽  
Author(s):  
Jiri Kalabis ◽  
Gang Li ◽  
Mizuho Fukunaga-Kalabis ◽  
Anil K. Rustgi ◽  
Meenhard Herlyn
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Organotypic Culture ◽  
Goblet Cells ◽  
Endothelin Receptors ◽  
Colonic Epithelium ◽  
Colonic Epithelial Cell ◽  
Colonic Epithelial Cells ◽  
Endothelin 3 ◽  
Human Colonic Epithelial Cell

Cells within the normal human colonic epithelium undergo a dynamic cycle of growth, differentiation, and death. The organotypic culture system of human fetal colonic epithelial cells seeded on top of collagen gels with embedded colonic fibroblasts allowed prolonged culture of the colonic epithelial cells (Kalabis J, Patterson MJ, Enders GM, Marian B, Iozzo RV, Rogler G, Gimotty PA, Herlyn M. FASEB J 17: 1115–1117, 2003). Herein, we have evaluated the role of endothelin-3 (ET3) and both cognate endothelin receptors (ETRA, ETRB) for human colonic epithelial cell growth and survival. ET3 was produced continuously by the fibroblasts as a result of adenovirus-mediated gene transfer. The presence and function of the endothelin receptors (ETRs) in epithelial cells was evaluated by [3H]thymidine incorporation using primary epithelial cells in monoculture and by immunohistochemistry on human fetal and adult paraffin-embedded tissues. In organotypic culture, ET3 increased the number of goblet cells but not of enteroendocrine cells. The increase in goblet cells was caused by prolonged cell survival and differentiation. The inhibition of both ETRA and ETRB significantly decreased the number of goblet cells and proliferation in epithelial cells, whereas the number of enteroendocrine cells remained unchanged. ET3 induced activation of IκB and MAPK in the epithelial cells, suggesting that these signaling pathways mediate its proproliferation and prosurvival activities. Our results demonstrate that ET3 is involved in regulating human colonic epithelial cell proliferation and survival, particularly for goblet cells, and may be an important component of colonic homeostasis.

Rapid effects of steroid hormones on free intracellular calcium in T84 colonic epithelial cells

1996 ◽  
Vol 271 (6) ◽  
pp. C1935-C1941 ◽  
Author(s):  
C. M. Doolan ◽  
B. J. Harvey
Keyword(s):  
Epithelial Cells ◽  
Epithelial Cell Line ◽  
Colonic Epithelium ◽  
Bathing Solution ◽  
Krebs Solution ◽  
Colonic Epithelial Cell ◽  
Colonic Epithelial Cells ◽  
Colonic Epithelial Cell Line ◽  
Free Intracellular Calcium ◽  
Human Colonic Epithelial Cell

Studies from our laboratory have demonstrated rapid (< 1 min) nongenomic activation of K+ recycling and Na+/H+ exchange by mineralocorticoids in human colonic epithelium, and studies from other laboratories have demonstrated rapid effects of aldosterone on intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells. Here a rapid nongenomic effect of aldosterone on [Ca2+]i is demonstrated in the human colonic epithelial cell line T84. Aldosterone induced a rapid increase in [Ca2+]i within approximately 2 min. The rise in [Ca2+]i after aldosterone appears to result from the activation of a Ca2+ influx pathway, inasmuch as 1) no increase in [Ca2+]i was observed with aldosterone when cells were bathed in Ca(2+)-free Krebs solution and 2) emptying of the intracellular Ca2+ stores by thapsigargin was not enhanced by addition of aldosterone to extracellular Ca(2+)-free solution. In contrast, the Ca2+ response to aldosterone, in the presence of 2 mM Ca2+ in the external bathing solution, was not decreased after intracellular Ca2+ stores were emptied by thapsigargin. Other mineralocorticoid hormones increased [Ca2+]i, whereas the glucocorticoid hydrocortisone failed to increase [Ca2+]i. These results demonstrate the existence of a mineralocorticoid-specific Ca(2+)-signaling pathway in human colonic T84 (crypt) epithelial cells.

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.

S1788 Glycine and Glutamine Down-Regulate IL-6-Induced Claudin-2 Expression in Human Colonic Epithelial Cell Monolayers

2010 ◽  
Vol 138 (5) ◽  
pp. S-274
Author(s):  
Yoshie Takahashi ◽  
Tomoo Nakagawa ◽  
Xianzhi Zhang ◽  
Yoshiko Noguchi ◽  
Toru Sato ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Colonic Epithelial Cell ◽  
Cell Monolayers ◽  
Epithelial Cell Monolayers ◽  
Human Colonic Epithelial Cell
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