Temporal response of uterine prostaglandins to estradiol treatment in the ovariectomized-prenant rat

Wilson, Laird; Huang, Lan

doi:10.1016/0090-6980(84)90117-5

Cited by 12 publications

(2 citation statements)

References 14 publications

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“…Estradiol was reported to increase the release of arachidonate, the precursor of prostaglandins, via its effect on phospholipase A 2 (37,38). Steroids are known to regulate prostaglandin synthesis at the prostaglandin G/H synthase level (19,39) and at steps subsequent to the formation of prostaglandin G and H (21,22). Thus, it appeared possible that in the uropygial glands, estrogen might regulate prostaglandin metabolism, resulting in the increased production of a PPAR␥ ligand.…”

mentioning

confidence: 99%

Estrogen-induced Production of a Peroxisome Proliferator-activated Receptor (PPAR) Ligand in a PPARγ-expressing Tissue

Ma¹,

Sprecher²,

Kolattukudy³

1998

Journal of Biological Chemistry

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Peroxisome proliferation has been associated with carcinogenesis in the liver, and estrogen intake has been associated with increased risk of cancer in the hormone target tissues. Estrogen-induced peroxisome proliferation has been observed in an estrogen target tissue, the uropygial gland in the duck. To elucidate the molecular mechanism of this process, we previously isolated the cDNA of peroxisome proliferator-activated receptor ␥1 (PPAR␥1) from the duck uropygial gland and found that its expression was high exclusively in this tissue of duck. However, the nature of the ligand for PPAR␥1 and how estrogen might enhance PPAR␥1-regulated gene expression were not known. Here we demonstrate that estrogen treatment of animals enhanced the metabolism of arachidonic acid in the uropygial gland. Conversion of prostaglandin D 2 to a metabolite was induced by estradiol treatment preceding peroxisome proliferation. High performance liquid chromatography and TLC analyses showed that the metabolite behaved chromatographically similar to prostaglandin J 2 and ⌬ 12 -prostaglandin J 2 . Gas chromatography/mass spectrometry revealed a striking similarity of the metabolite to ⌬ 12 -prostaglandin J 2 , the only form among the J 2 series whose natural occurrence has been detected. Furthermore, this metabolite was able to activate duck PPAR␥1 to the same extent as the same concentrations of ⌬ 12 -prostaglandin J 2 and 15-deoxy-⌬ 12,14 -prostaglandin J 2 , whereas under the same conditions, prostaglandin D 2 was not effective. The results suggest that estrogen treatment induced the formation of a prostaglandin D 2 metabolite that activated duck PPAR␥1, causing the induction of peroxisome proliferation in the duck uropygial gland.Tumor formation in human tissues such as the breast, endometrium, and ovary has been correlated with estrogen intake. Despite extensive investigations, how estrogens may enhance the incidence of cancer in the hormone target tissues remains unknown. Peroxisome proliferation has been thought to be causally related to tumor formation in rodent liver because peroxisome proliferation caused by a large variety of proliferators correlates well with hepatic tumor formation, presumably through oxidative damage to DNA caused by the production of oxidants produced by peroxisomal oxidase(s) (1-3). Estradiol administration to mallard ducks induces peroxisome proliferation in an estrogen target tissue, the uropygial gland (4). These observations raise the possibility that in mammalian tissues that are estrogen targets, peroxisome proliferation might be triggered by exogenous estrogens, leading to carcinogenesis.How estrogen causes peroxisome proliferation is unknown. Peroxisome proliferator-activated receptors (PPARs) 1 are a group of nuclear receptors involved in mediating peroxisome proliferation. Among the three subtypes (␣, ␤, and ␥) of PPAR, the ␣ form is most responsive to peroxisome proliferators and is the primary form for the pleiotropic responses in rodents (5, 6). A recent study revealed that leukotriene B 4 ...

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confidence: 99%

Estrogen-induced Production of a Peroxisome Proliferator-activated Receptor (PPAR) Ligand in a PPARγ-expressing Tissue

Ma¹,

Sprecher²,

Kolattukudy³

1998

Journal of Biological Chemistry

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“…For example, PPAR-γ is activated by prostaglandins, and especially the J2 series of prostaglandins [35] . Estrogen regulates the synthesis of prostaglandins in the target tissues such as uterus [36] . Estradiol increases arachidonate which is one of precursor of the prostaglandins [37] .…”

Section: Discussionmentioning

confidence: 99%

The Effects of Gemfibrozil and Ovariectomy on the Peroxisome Proliferator Activated Receptors (PPARs) in Mice with Experimentally Induced Obesity

Tunca¹,

Devrim²,

Sözmen³

et al. 2013

Kafkas Univ Vet Fak Derg

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Initiation of Parturition

Liggins

1994

Marshall’s Physiology of Reproduction

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Temporal response of uterine prostaglandins to estradiol treatment in the ovariectomized-prenant rat

Cited by 12 publications

References 14 publications

Estrogen-induced Production of a Peroxisome Proliferator-activated Receptor (PPAR) Ligand in a PPARγ-expressing Tissue

Estrogen-induced Production of a Peroxisome Proliferator-activated Receptor (PPAR) Ligand in a PPARγ-expressing Tissue

The Effects of Gemfibrozil and Ovariectomy on the Peroxisome Proliferator Activated Receptors (PPARs) in Mice with Experimentally Induced Obesity

Initiation of Parturition

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