Prostaglandin E2 Down-Regulates the Expression of HLA-DR Antigen in Human Colon Adenocarcinoma Cell Lines

Arvind, Padma; Papavassiliou, Efstathios; Tsioulias, George J.; Qiao, Liang; Lovelace, Christopher I.P.; Duceman, Barry W.; Rigas, Basil

doi:10.1021/bi00016a035

Cited by 33 publications

(15 citation statements)

References 32 publications

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“…Again, the cells of the inflamed tissue or organ can also produce and respond to the prostanoids, providing an additional mechanism by which these lipid mediators may affect the course of the chronic inflammatory response. For example, prostanoids can alter the production of cytokines by epithelial cells and alter the expression of class II MHC antigens by antigen-presenting cells, thus modulating the course and resolution of the response (40).…”

Section: Identification Of Prostanoid Pathways Modulating Specific Immentioning

confidence: 99%

Mixed messages: modulation of inflammation and immune responses by prostaglandins and thromboxanes

Tilley¹,

Coffman²,

Koller³

2001

J. Clin. Invest.

386

385

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Prostaglandins and their precursorsVirtually every organism has evolved mechanisms by which, upon stimulation, lipids are released from plasma membranes and metabolized into mediators capable of changing cellular physiology. As these lipids are present at the first site exposed to external challenge, they provide an ideal substrate for the synthesis of defensive mediators and homeostatic regulators. One such group of lipid mediators is the prostanoids, including the prostaglandins (PGs) and thromboxanes (TXs).Soon after their initial isolation and characterization, the ability of prostanoids to influence inflammation and immune responses was recognized. For example, administration of prostanoids, either alone or in combination, could reproduce the cardinal signs of inflammation. Because they could induce inflammatory changes when injected into tissue and were present at high levels in inflamed lesions, prostanoids were initially categorized as proinflammatory mediators. As our understanding of prostanoid physiology has evolved, it has become clear that these mediators can act to both promote and inhibit inflammation. Thus, it is more accurate to envision these molecules as part of a complex regulatory network that modulates the actions of immune cells and the surrounding microenvironment. Their overall impact in an individual inflammatory response will depend on several factors, including the level of immune cell activation, the presence of other mediators, and the physiological state of the organism.Our ability to dissect the role of prostanoids in complex inflammatory responses has been substantially advanced by the recent development of mouse lines with targeted mutations of genes encoding enzymes and receptors in the prostanoid pathway. In this review we will develop the concept that prostanoids are both effectors and regulators of inflammation, emphasizing new information provided by these mouse models. Production of prostanoids during inflammationProstanoids are produced when arachidonic acid (AA) is released from the plasma membrane by phospholipases and metabolized by cyclooxygenases (COXs) and specific isomerases. During an inflammatory response, both the level and the profile of prostanoid production can change dramatically. While prostanoid levels are generally very low in uninflamed tissues, they increase

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Section: Identification Of Prostanoid Pathways Modulating Specific Immentioning

confidence: 99%

Mixed messages: modulation of inflammation and immune responses by prostaglandins and thromboxanes

Tilley¹,

Coffman²,

Koller³

2001

J. Clin. Invest.

386

385

View full text Add to dashboard Cite

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“…In addition, PGE 2 increases the motility and metastatic potential of cancer cells [59,72]. PGE 2 can also lead to a local immunosuppression that favors tumor development [3,38]. Finally, COX-2 expression induces angiogenesis [73].…”

Section: Main Characteristics Of Cyclooxygenasesmentioning

confidence: 99%

Cyclooxygenase-2 and its role in colorectal cancer development

et al. 2004

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Cyclooxygenase 2 (COX-2), also called prostaglandin endoperoxide synthase 2, is involved in colorectal tumor development. This review deals with particular questions raised in this field such as the mechanisms of COX-2 related tumor promotion, the role of the different types of cells (epithelial and interstitial) expressing COX-2, the factors that trigger COX-2 induction, and the clinical potential of selective COX-2 inhibitors to treat or prevent colorectal tumors. Several mechanisms of COX-2 related tumor promotion have been identified. Some are dependent on prostaglandin E(2) production (such as induction of cell proliferation, angiogenenis or local immunosuppression, inhibition of apoptosis, increase in cell motility) and others are not (such as carcinogen activation or malondialdehyde production). COX-2 expression has been demonstrated in epithelial cells of colorectal cancers and adenomas and also in interstitial cells. These cells correspond to macrophages and/or fibroblasts and endothelial cells. COX-2 expression in these interstitial cells participates in tumor development. Factors or events that trigger COX-2 expression include oncogene activation, antioncogene inactivation, cytokines, growth factors, some fatty acids, bile salts, and mucins. Finally, selective COX-2 inhibitors may be effective in preventing or treating colorectal adenomas or carcinomas. However, their real efficiency and the cost/benefit balance are currently evaluated, and no definite conclusion can be made at the moment.

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“…LLC, Vancouver, WA, USA) [24], glutathione peroxidase activity with assay kit (Oxis International, Inc., Foster City, CA, USA) [25], catalase activity with catalase assay kit (Cayman Chemical Co., Ann Arbor, MI, USA) [26], and superoxide dismutase activity with superoxide dismutase assay kit-WST (Dojindo Molecular Technologies, Inc., Gaithersburg, MD, USA) [27], amount of prostaglandin E2 and thromboxane B2 with enzyme immunoassay kit (Cayman Chemical Co.) [28,29]. Superoxide dismutase activity was expressed as units per mg protein, and one unit was defined as the amount of superoxide dismutase required to inhibit the rate of cytochrome c reduction by 50%.…”

Section: Collection Of Colon Tissue Samples At 44 Weeksmentioning

confidence: 99%

Long-term ingestion of reduced glutathione suppressed an accelerating effect of beef tallow diet on colon carcinogenesis in rats

et al. 2009

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This study indicated that GSH suppressed the number of ACF, but the attenuation of colon carcinogenesis was limited to the number of colon cancers, although anti-oxidative effects and suppressive effects of arachidonic acid cascade were demonstrated by several indexes. These results suggested that colon carcinogenesis enhanced by beef tallow was partly caused by oxidative stress and arachidonic acid cascade, which were reduced by GSH.

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Prostaglandin E2 Down-Regulates the Expression of HLA-DR Antigen in Human Colon Adenocarcinoma Cell Lines

Cited by 33 publications

References 32 publications

Mixed messages: modulation of inflammation and immune responses by prostaglandins and thromboxanes

Mixed messages: modulation of inflammation and immune responses by prostaglandins and thromboxanes

Cyclooxygenase-2 and its role in colorectal cancer development

Long-term ingestion of reduced glutathione suppressed an accelerating effect of beef tallow diet on colon carcinogenesis in rats

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