A PPAR-independent pathway to PUFA-induced COX-2 expression
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135 citations
Cites background from "A PPAR-independent pathway to PUFA-..."
...MG-132 (47, 69, 70) In vitro, EEC Y IL-6 and LIF In vitro, bovine ESC Y PTGS-2 and COX-2 Parthenolide (69) In vitro, bovine ESC Y PTGS-2 SN-50 (33, 47) In vitro, EEC Y IL-6 and LIF In vivo, nude mouse Y Ec lesion development Y ICAM-1 and [ apoptosis Curcumin (53, 54, 67, 168) In vitro, ESC and EcSC Y MIF In vivo, human Unknown, Y symptoms? Sulindac (55) In vitro, ESC Y RANTES Thalidomide (62) In vitro, EcSC Y IL-8 TPCK (59) In vitro, EcSC Y IL-8 GnRH-a (59) In vivo, human/in vitro, EcSC Y IL-8...
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...The most accepted hypothesis on the origin of peritoneal endometriosis postulates that this disease originates from regurgitated menstrual endometrial cells (ECs) able to survive, adhere, invade, and proliferate in the peritoneal cavity (5–9)....
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...In vitro studies in stimulated ECs and EcCs testing different NF-kB inhibitors—including MG132, parthenolide, SN-50, BAY 11-7085, curcumin, sulindac, thalidomide, N-tosyl-l-phenylalanine chloromethyl ketone (TPCK), GnRH agonists, progesterone, progestational compounds, IKK-2 inhibitor, PPAR-g ligand (pioglitazone), IL-10, and NF-kB decoy oligonucleotides (ODNs)—have shown a reduction in proinflammatory, growth, and invasion mediators COX-2, IL-6, leukemia inhibitory factor (LIF), MIF, RANTES, IL-8, MCP-1, GM-CSF, ICAM-1, and MMP-9, have reduced cell proliferation, monocyte chemotactic activity, and cell invasion, and have increased apoptosis as a result of decreased NF-kB activation (33, 47, 53–55, 59, 62–64, 67–70, 87, 88, 159, 160)....
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...Further studies are needed to understand the complex genomic and nongenomic interactions between estrogen and progesterone, their receptors, NF-kB, and other pathways in ECs and EcCs....
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...In vitro studies have revealed constitutive and inducible activation of NF-kB in ECs....
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99 citations
37 citations
Cites background from "A PPAR-independent pathway to PUFA-..."
...Recent data suggest that the proteasome inhibitor MG132 prevents fatty acid induction of the pro-inflammatory enzyme cyclooxygenase-2 in endometrial stromal cells [23]....
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30 citations
Cites background from "A PPAR-independent pathway to PUFA-..."
...However, PPARG-independent effects also cannot be denied completely as PUFAs are known to take PPAR-independent pathways (Derecka et al. 2008) and also PPARG inhibitor (GW9662) inhibited the cell growth of human tumor mammary cell line, which supports the existence of PPARG-independent pathways…...
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22 citations
Cites background from "A PPAR-independent pathway to PUFA-..."
...It has been found previously that PKC activators, such as PMA, induced COX-2 expression in ESC [57]....
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References
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