Interaction between uterine PGE and PGF2α production and the nitridergic system during embryonic implantation in the rat

Novaro, Virginia; Rettori, Valéria; González, Ezequiel; Jawerbaum, Alicia; Faletti, A.; Canteros, Griselda; Gimeno, M.F.

doi:10.1016/0090-6980(96)00043-3

Cited by 52 publications

(20 citation statements)

References 24 publications

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“…It has been assumed that NO directly influences the activity of hemecontaining enzymes such as cyclooxygenase [32] and modulates PGF 2␣ production in reproductive organs, including the uterus [33][34][35]. Our present results provide some evidence that the TNF␣-stimulated PGF 2␣ production is in part mediated by induction of NOS activity and the subsequent NO-cGMP generation.…”

Section: Discussionsupporting

confidence: 51%

Production of Prostaglandin F2α by Cultured Bovine Endometrial Cells in Response to Tumor Necrosis Factor α: Cell Type Specificity and Intracellular Mechanisms1

Skarzynski

Miyamoto

Okuda

2000

Biology of Reproduction

149

133

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Tumor necrosis factor alpha (TNFalpha) has been shown to be a potent stimulator of prostaglandin (PG) F(2alpha) secretion in the bovine endometrium. The aims of the present study were to determine the cell types in the endometrium (epithelial or stromal cells) responsible for the secretion of PGF(2alpha) in response to TNFalpha, and the intracellular mechanisms of TNFalpha action. Cultured bovine epithelial and stromal cells were exposed to TNFalpha (0.006-6 nM) or oxytocin (100 nM) for 4 h. TNFalpha resulted in a dose-dependent increase of PGF(2alpha) production in the stromal cells (P < 0.001) but not in the epithelial cells. On the other hand, oxytocin stimulated PGF(2alpha) output in the epithelial cells but not in the stromal cells. When the stromal cells were incubated for 24 h with TNFalpha and inhibitors of phospholipase (PL) C or PLA(2), only PLA(2) inhibitor completely stopped the actions of TNFalpha (P < 0.001). When the stromal cells were exposed to TNFalpha and arachidonic acid, the action of TNFalpha was augmented (P < 0.001). When the stromal cells were incubated for 24 h with a nitric oxide (NO) donor (S-NAP), S-NAP stimulated the PGF(2alpha) production dose-dependently. Although an NO synthase (NOS) inhibitor (L-NAME) reduced TNFalpha-stimulated PGF(2alpha) production, an inhibitor of phosphodiesterase augmented the actions of TNFalpha and S-NAP (P < 0. 05). The overall results indicate that the target of TNFalpha for stimulation of PGF(2alpha) production in cattle is the endometrial stromal cells, and that the actions of TNFalpha are mediated via the activation of PLA(2) and arachidonic acid conversion. Moreover, TNFalpha may exert a stimulatory effect on PGF(2alpha) production via the induction of NOS and the subsequent NO-cGMP formation.

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Section: Discussionsupporting

confidence: 51%

Production of Prostaglandin F2α by Cultured Bovine Endometrial Cells in Response to Tumor Necrosis Factor α: Cell Type Specificity and Intracellular Mechanisms1

Skarzynski

Miyamoto

Okuda

2000

Biology of Reproduction

149

133

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“…uterus during implantation of the embryos. Uterine PGE 2 and NO increase during the peri-implantation days in rats, probably as a result of an increase of the plasma oestradiol levels, and they diminish after the implantation period [84,85]. In the uterus of mild diabetic rats, PGE 2 was increased during the peri-implantation period when compared to controls, and there was no return to preimplantation levels after implantation [44] (Fig.…”

Section: Effects Of Maternal Hyperglycemia During Pre-implantation Anmentioning

confidence: 89%

The Role of Alterations in Arachidonic Acid Metabolism and Nitric Oxide Homeostasis in Rat Models of Diabetes During Early Pregnancy

Jawerbaum¹,

González

2005

CPD

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The diabetic pathology induces reproductive abnormalities that enhance spontaneous abortion, congenital anomalies and neonatal morbidity/mortality rates, abnormalities that begin with an altered female gamete. In this review we focus on the damage induced by maternal hyperglycemia during ovulation, early embryo development, implantation and embryo organogenesis in experimental rat models of diabetes. Hyperglycemia can induce cellular damage by enhancing the production of reactive oxygen species (ROS), by altering arachidonic acid metabolism (thus leading to altered production of prostaglandins such us PGE(2)and 15deoxydelta(12-14)PGJ(2), involved in signalling and developmental pathways), and by enhancing the generation of nitric oxide (a mediator of many cell functions including apoptotic cell death). In maternal diabetes all of these abnormalities are present from the oocyte stage, during embryonic implantation, and during embryo organogenesis. The involvement of these alterations in embryo loss and congenital malformations due to diabetes and the cross-talk among these metabolic pathways are discussed. As maternal hyperglycemia induces damage from the oocyte stage and throughout embryo development the data reviewed suggests the need of strict preconceptional metabolic control. The importance of the molecules involved in hyperglycemia-induced damage as future pharmacological targets for intervention is discussed.

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“…It has been shown that NO activates COX, an important transduction mechanism for NO actions in many tissues and organs. 23 37 38 In addition, endogenous NO has been shown to have a critical role in the stimulation of COX-2 in the mouse macrophage cell line RAW 264. 7,24 probably interacting with the iron-haem centre at the active site of COX-2, leading to the activation of COX enzymes through soluble guanylase cyclase.…”

Section: Discussionmentioning

confidence: 99%

“…Given the bank of reports supporting interaction between these pathways, [22][23][24][25][26][27][28] we further investigated the hypothesis that combined inhibition of both nitrergic and prostanoid pathways may offer enhanced anti-inflammatory benefit.…”

mentioning

confidence: 99%

Divergent roles of nitrergic and prostanoid pathways in chronic joint inflammation

Day

Lockhart²,

Ferrell

et al. 2004

Annals of the Rheumatic Diseases

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Background: Nitrergic and prostanoid pathways have both been implicated in inflammatory processes. Objective: To investigate their respective contributions in a rat model of chronic arthritis. Methods: Male Wistar rats (n = 4-6/group) received either an intra-articular injection of 2% carrageenan/4% kaolin (C/K) or intra-and periarticular injections of Freund's complete adjuvant (FCA; 10 mg/ml M tuberculosis). Joint diameter, urinary nitric oxide metabolites (NO x ), and prostaglandin E 2 (PGE 2 ) levels were measured as indices of the inflammatory process. A prophylactic and therapeutic (day 5) dose ranging study of an inducible nitric oxide synthase inhibitor, L-N-(1-iminoethyl)-lysine (L-NIL), and a cyclo-oxygenase-2 (COX-2) inhibitor, SC-236, was performed with the drugs given subcutaneously. Submaximal doses were identified and used for combination studies. Appropriate vehicle controls were included. Results: L-NIL and SC-236 dose dependently inhibited C/K induced acute joint swelling, the magnitude being greatest when they were given in combination. Both prophylactic and therapeutic administration of SC-236 in the FCA induced model of chronic arthritis produced a dose dependent reduction in all the measures assessed. However, although L-NIL demonstrated similar dose dependent inhibition of urinary NO x and PGE 2 levels, joint swelling was significantly exacerbated in this model. Co-administration of the inhibitors nullified the benefits of SC-236. Conclusion: Whereas COX-2 derived prostaglandins are proinflammatory in both acute and chronic joint inflammation, NO seems to have divergent roles, being anti-inflammatory in chronic and proinflammatory in acute joint inflammation.

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Interaction between uterine PGE and PGF2α production and the nitridergic system during embryonic implantation in the rat

Cited by 52 publications

References 24 publications

Production of Prostaglandin F2α by Cultured Bovine Endometrial Cells in Response to Tumor Necrosis Factor α: Cell Type Specificity and Intracellular Mechanisms1

Production of Prostaglandin F2α by Cultured Bovine Endometrial Cells in Response to Tumor Necrosis Factor α: Cell Type Specificity and Intracellular Mechanisms1

The Role of Alterations in Arachidonic Acid Metabolism and Nitric Oxide Homeostasis in Rat Models of Diabetes During Early Pregnancy

Divergent roles of nitrergic and prostanoid pathways in chronic joint inflammation

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