Expression of prostaglandin endoperoxide H synthase‐2 induced by nitric oxide in conditionally immortalized murine colonic epithelial cells

2000 ◽  
Vol 14 (9) ◽  
pp. 1188-1201 ◽  
Author(s):  
Jay M. Mei ◽  
Norman G. Hord ◽  
Dolores F. Winterstein ◽  
Steven P. Donald ◽  
James M. Phang
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Colonic Epithelial Cells ◽  
Prostaglandin Endoperoxide ◽  
Endoperoxide H Synthase

The Cytotoxic Effects of Nitric Oxide on HT29 Colonic Epithelial Cells

1997 ◽  
Vol 93 (s37) ◽  
pp. 16P-16P
Author(s):  
PJ Roberts ◽  
M Shorthouse ◽  
JO Hunter ◽  
SJ Middleton
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Colonic Epithelial Cells ◽  
Cytotoxic Effects

Interaction of Nitric Oxide with Prostaglandin Endoperoxide H Synthase-1:  Implications for Fe−His Bond Cleavage in Heme Proteins†

2000 ◽  
Vol 104 (46) ◽  
pp. 10844-10850 ◽  
Author(s):  
Johannes P. M. Schelvis ◽  
Steve A. Seibold ◽  
Jose F. Cerda ◽  
R. Michael Garavito ◽  
Gerald T. Babcock
Keyword(s):  
Nitric Oxide ◽  
Heme Proteins ◽  
Bond Cleavage ◽  
Prostaglandin Endoperoxide ◽  
Endoperoxide H Synthase

Prostaglandin endoperoxide H synthase expression in human thyroid epithelial cells

2001 ◽  
Vol 280 (3) ◽  
pp. C701-C708 ◽  
Author(s):  
Andrew G. Gianoukakis ◽  
H. James Cao ◽  
Timothy A. Jennings ◽  
Terry J. Smith
Keyword(s):  
Epithelial Cells ◽  
Culture Conditions ◽  
Control Culture ◽  
Human Thyroid ◽  
Prostaglandin E ◽  
Glucocorticoid Treatment ◽  
Functional Roles ◽  
Prostaglandin Endoperoxide ◽  
Endoperoxide H Synthase ◽  
Cyclooxygenase Isoforms

KAT-50, an established human thyrocyte cell line, expresses constitutively high levels of prostaglandin endoperoxide H synthase-2 (PGHS-2), the inflammatory cyclooxygenase. Here, we examine primary human thyrocytes. We find that they, too, express PGHS-2 mRNA and protein under control culture conditions. A substantial fraction of the basal prostaglandin E2(PGE2) produced by these cells can be inhibited by SC-58125 (5 μM), a PGHS-2-selective inhibitor. Interleukin (IL)-1β (10 ng/ml) induces PGHS-2 expression and PGE2 production in primary thyrocytes. The induction of PGHS-2 and PGE2synthesis by IL-1β could be blocked by glucocorticoid treatment. Unlike KAT-50, most of the culture strains also express PGHS-1 protein. Our observations suggest that both cyclooxygenase isoforms may have functional roles in primary human thyroid epithelial cells, and PGHS-2 might predominate under basal and cytokine-activated culture conditions.

scholarly journals Dietary Salt Administration Decreases Enterotoxigenic Bacteroides fragilis (ETBF)-Promoted Tumorigenesis via Inhibition of Colonic Inflammation

2020 ◽  
Vol 21 (21) ◽  
pp. 8034
Author(s):  
Soonjae Hwang ◽  
Hye Chin Yi ◽  
Samnoh Hwang ◽  
Minjeong Jo ◽  
Ki-Jong Rhee
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Bacteroides Fragilis ◽  
Serum Levels ◽  
Colonic Polyp ◽  
Dietary Salt ◽  
Colonic Epithelial Cells ◽  
Beneficial Effects ◽  
Colon Inflammation ◽  
Oxide Synthase

Consumption of a Western-type diet has been linked to gut-microbiota-mediated colon inflammation that constitutes a risk factor for colorectal cancer. A high salt diet (HSD) exacerbates IL-17A-induced inflammation in inflammatory bowel disease and other autoimmune diseases. Enterotoxigenic Bacteroides fragilis (ETBF) is a gut commensal bacterium and reported to be a potent initiator of colitis via secretion of the Bacteroides fragilis toxin (BFT). BFT induces ectodomain cleavage of E-cadherin in colonic epithelial cells, consequently leading to cell rounding, epithelial barrier disruption, and the secretion of IL-8, which promotes tumorigenesis in mice via IL-17A-mediated inflammation. A HSD is characteristic of the Western-type diet and can exhibit inflammatory effects. However, a HSD induces effects in ETBF-induced colitis and tumorigenesis remain unknown. In this study, we investigated HSD effects in ETBF-colonized mice with azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced tumorigenesis as well as ETBF colitis mice. Unexpectedly, ETBF-infected mice fed a HSD exhibited decreased weight loss and splenomegaly and reduction of colon inflammation. The HSD significantly decreased the expression of IL-17A and inducible nitric oxide synthase (iNOS) in the colonic tissues of ETBF-infected mice. In addition, serum levels of IL-17A and nitric oxide (NO) were also diminished. However, HT29/C1 colonic epithelial cells treated with sodium chloride showed no changes in BFT-induced cellular rounding and IL-8 expression. Furthermore, HSD did not affect ETBF colonization in mice. In conclusion, HSD decreased ETBF-induced tumorigenesis through suppression of IL-17A and iNOS expression in the colon. HSD also inhibited colonic polyp numbers in the ETBF-infected AOM/DSS mice. Taken together, these findings suggest that a HSD consumption inhibited ETBF-promoted colon carcinogenesis in mice, indicating that a HSD could have beneficial effects under certain conditions.

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