Transcriptional regulation of genes for enzymes of the prostaglandin biosynthetic pathway

Lindström, Tamsin M.; Bennett, Phillip R.

doi:10.1016/j.plefa.2003.04.003

Cited by 30 publications

(24 citation statements)

References 248 publications

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“…The effect of TNF-α is partially mediated by PLA 2 and COX-2, which promote a shift towards a proinflammatory lipid profile (e.g., leukotriene B 4 and PGE 2 ) to further perpetuate inflammatory responses [6,43]. The induction of PLA 2 and COX-2 can be mediated through NF-κB and MAPK signaling in response to TNF-α.…”

Section: Discussionmentioning

confidence: 99%

“…The substrate AA is then converted into prostaglandins and leukotrienes by the cyclooxygenase (e.g., via the COX-1 and COX-2) and lipoxygenase pathways, respectively [5]. The induction of PLA 2 and COX-2 is highly regulated through mitogen-activated protein kinases (MAPKs), nuclear factor-kappa B (NF-κB), and other pathways [6], and can be stimulated by cytokines and trauma [5]. In turn, prostaglandins, especially prostaglandin E 2 (PGE 2 ), can modulate inflammatory responses by regulating cytokine production and leukocyte activation [1,7].…”

Section: Introductionmentioning

confidence: 99%

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Alteration in the activation state of new inflammation-associated targets by phospholipase A2-activating protein (PLAA)

Zhang

Sha

Wood

et al. 2008

Cellular Signalling

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Phospholipase A 2 (PLA 2 )-activating protein (PLAA) is a novel signaling molecule that regulates the production of prostaglandins (PGE 2 ) and tumor necrosis factor (TNF)-α. To characterize the function of native PLAA in situ, we generated HeLa (Tet-off) cells overexpressing plaa (plaa high ) and control (plaa low ) cells, with the plaa gene in opposite orientation in the latter construct. The plaa high cells produced significantly more PGE 2 and interleukin (IL)-6 compared to plaa low cells in response to TNF-α. There was increased activation and/or expression of cytosolic PLA 2 , cyclooxgenase-2, and NF-κB after induction of plaa high cells with TNF-α compared to the respective plaa low cells. Microarray analysis of plaa high cells followed by functional assays revealed increased production of proinflammatory cytokine IL-32 and a decrease in the production of annexin A4 and clusterin compared to plaa low cells. We demonstrated the role of annexin A4 as an inhibitor of PLA 2 and showed that addition of exogeneous clusterin limited the production of PGE 2 from plaa high cells. To understand regulation of plaa gene expression, we used a luciferase reporter system in HeLa cells and identified one stimulatory element, with Sp1 binding sites, and one inhibitory element, in exon 1 of the plaa gene. By using decoy DNA oligonucleotides to Sp1 and competitive binding assays, we showed that Sp1 maintains basal expression of the plaa gene and binds to the above-mentioned stimulatory element. We demonstrated for the first time that the induction of native PLAA by TNF-α can perpetuate inflammation by enhancing activation of PLA 2 and NF-κB.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alteration in the activation state of new inflammation-associated targets by phospholipase A2-activating protein (PLAA)

Zhang

Sha

Wood

et al. 2008

Cellular Signalling

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“…Down-regulation of GILZ in the decidua may also play a role in the parturition cascade through its regulation of nuclear factor kappa B (NF-kB) (Lindstrom & Bennett 2004). In vitro, GILZ co-immunoprecipitates with p65, which would inhibit transactivation of NF-kB (Lindstrom & Bennett 2004).…”

Section: Implantation-site Transcription Factors 565mentioning

confidence: 99%

“…In vitro, GILZ co-immunoprecipitates with p65, which would inhibit transactivation of NF-kB (Lindstrom & Bennett 2004). Release of GILZ's inhibition (by downregulation of GILZ) of NF-kB may play an important role in the parturition cascade.…”

Section: Implantation-site Transcription Factors 565mentioning

confidence: 99%

“…Release of GILZ's inhibition (by downregulation of GILZ) of NF-kB may play an important role in the parturition cascade. The murine and human COX-2 promoters contain a conserved pair of NF-kB-binding sites (Lindstrom & Bennett 2004). NF-kB activation of COX-2 has been shown in immortalized myometrial cells, WISH cells (immortalized amniotic cells) and in amniotic cells during labor (Wang & Tai 1998, Belt et al 1999, Allport et al 2001.…”

Section: Implantation-site Transcription Factors 565mentioning

confidence: 99%

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Identification of transcription factors at the site of implantation in the later stages of murine pregnancy

Zhao¹,

Koon²,

Bethin³

2006

Reproduction

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Despite medical advances, preterm delivery continues to complicate 12% of all births in the United States and is a major cause of neonatal deaths. One of the reasons that preterm labor continues to be a significant problem is that very little is understood about the factors involved in normal labor. Many investigators have studied parturition in the mouse and defined essential pathways for normal labor. Prostaglandins play an essential role in mouse labor and are important in human labor as well. We examined the 23 transcription factors from pregnant mouse uterus that change expression after the induction of cyclooxygenase-1, the enzyme that catalyzes the first committed step in prostaglandin synthesis. Using in situ hybridization, we have identified three of these transcription factors, Hoxa10, Hoxa11 and GILZ as being expressed in the decidua and regulated at the end of pregnancy. Both Hoxa10 and Hoxa11 are known to be critical for implantation, but very little is known about their roles in late gestation. GILZ has not previously been identified in the gravid uterus. In summary, we have identified three transcription factors that are regulated in the decidua at the end of pregnancy, suggesting a role in detachment of the fetus and placenta.

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Blood COX-2 and PGES gene transcription during the peripartum period of dairy cows with normal puerperium or with uterine infection

Silva

Gaivão

Leitão

et al. 2008

Domestic Animal Endocrinology

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Transcriptional regulation of genes for enzymes of the prostaglandin biosynthetic pathway

Cited by 30 publications

References 248 publications

Alteration in the activation state of new inflammation-associated targets by phospholipase A2-activating protein (PLAA)

Alteration in the activation state of new inflammation-associated targets by phospholipase A2-activating protein (PLAA)

Identification of transcription factors at the site of implantation in the later stages of murine pregnancy

Blood COX-2 and PGES gene transcription during the peripartum period of dairy cows with normal puerperium or with uterine infection

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