Kinetic effect of oestrogen on secretion of prostaglandins E2 and F2α in bovine oviduct epithelial cells

2017 ◽  
Vol 29 (3) ◽  
pp. 482 ◽  
Author(s):  
Zhiheng Dong ◽  
Nan Zhang ◽  
Wei Mao ◽  
Bo Liu ◽  
Na Huang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dynamic Change ◽  
Extracellular Fluid ◽  
Prostaglandin F2α ◽  
Subsequent Decrease ◽  
Polymerase Chain ◽  
Cox 2 ◽  
Oviduct Epithelial Cells ◽  
In Cell Western ◽  
Cox 1

This study aimed to investigate the effect of oestrogen on prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) secretion in bovine oviduct epithelial cells. Bovine oviduct epithelial cells were obtained from the lumen of fresh bovine oviducts. Quantitative real-time polymerase chain reaction and in-cell western assays were used to measure PGE2 and PGF2α synthase activity and enzyme-linked immunosorbent assays were used to detect the concentrations of the two prostaglandins in extracellular fluid. We observed that oestradiol caused a short-term increase in cyclo-oxygenase-2 (COX-2), which stimulated PGE2 and PGF2α secretion, and that a subsequent decrease in COX-2 and an increase in cyclo-oxygenase-1 (COX-1) produced a high PGE2 : PGF2α ratio. These findings reflect the dynamic change in PGE2 and PGF2α levels under the influence of oestrogen, which may be essential for fertilisation.

scholarly journals Intraluteal regulation of prostaglandin F2α-induced prostaglandin biosynthesis in pseudopregnant rabbits

Reproduction ◽  
2007 ◽  
Vol 133 (5) ◽  
pp. 1005-1016 ◽  
Author(s):  
M Zerani ◽  
C Dall’Aglio ◽  
M Maranesi ◽  
A Gobbetti ◽  
G Brecchia ◽  
...  
Keyword(s):  
Prostaglandin F2α ◽  
Enzymatic Activities ◽  
Synthesis Rate ◽  
Corpora Lutea ◽  
Positive Staining ◽  
Mrna Levels ◽  
Cox 2 ◽  
Pg E2 ◽  
Cox 1

The objective of the present study was to investigate in rabbit corpora lutea (CL), at both the cellular and molecular level, intraluteal cyclooxygenase (COX)-1, COX-2 and prostaglandin (PG) E2-9-ketoreductase (PGE2-9-K) enzymatic activities as well asin vitroPGE2 and PGF2α synthesis following PGF2α treatment at either early- (day-4) or mid-luteal (day-9) stage of pseudopregnancy. By immunohistochemistry, positive staining for COX-2 was localized in luteal and endothelial cells of stromal arteries at both the stages. In CL of both stages, basal COX-2 mRNA levels were poorly expressed, but rose (P< 0.01) 4- to 10-fold 1.5–6 h after treatment and then gradually decreased within 24 h. Compared to mid-stage, day-4 CL had lower (P< 0.01) COX-2 and PGE2-9-K basal activities, and PGF2α synthesis rate, but higher (P< 0.01) PGE2 production. Independent of luteal stage, PGF2α treatment did not affect COX-1 activity. In day-4 CL, PGF2α induced an increase (P< 0.01) in both COX-2 activity and PGF2α synthesis, whereas that of PGE2 remained unchanged. In day-9 CL, PGF2α up-regulated (P< 0.01) both COX-2 and PGE-9-K activities, and PGF2α production, but decreased (P< 0.01) PGE2 synthesis. All changes in gene expression and enzymatic activities occurred within 1.5 h after PGF2α challenge and were more marked in day-9 CL. Our data suggest that PGF2α directs intraluteal PG biosynthesis in mature CL, by affecting the CL biosynthetic machinery to increase the PGF2α synthesis in an auto-amplifying manner, with the activation of COX-2 and PGE-9-K; this may partly explain their differentially, age-dependent, luteolytic capacity to exogenous PGF2α in rabbits.

Prostaglandin endoperoxide synthase: why two isoforms?

1996 ◽  
Vol 270 (3) ◽  
pp. G393-G400 ◽  
Author(s):  
C. S. Williams ◽  
R. N. DuBois
Keyword(s):  
Epithelial Cells ◽  
Cardiac Fibrosis ◽  
Intestinal Epithelial Cells ◽  
Renal Dysplasia ◽  
Intestinal Epithelial ◽  
Phenotypic Changes ◽  
Prostaglandin Endoperoxide ◽  
Prostaglandin Endoperoxide Synthase ◽  
Cox 2 ◽  
Cox 1

Prostaglandin endoperoxide synthase-1 [prostaglandin G/H synthase-1 (PGHS-1)] and PGHS-2 are key enzymes in the conversion of arachidonic acid to prostaglandins and other eicosanoids. We refer to these isoforms as cyclooxygenase-1 (COX-1) and COX-2 in this review. This brief review focuses on recent developments in the study of these enzymes. Alterations in the expression levels of COX-2 result in distinct phenotypic changes in intestinal epithelial cells. Overexpression of COX-2 in intestinal epithelial cells results in increased adhesion to extracellular matrix proteins and inhibition of apoptosis. Disruption of the COX-2 gene in mice results in renal dysplasia, cardiac fibrosis, and defects in the ovary. Interestingly, disruption of the COX-1 gene results in distinct phenotypic changes different from those observed for COX-2. COX-1 null mice survive well, have no gastric pathology, and show less indomethacin-induced gastric ulceration than wild-type mice. These two closely related enzymes must have distinct functions in the organisms, since lack of their expression causes distinct phenotypic changes for each respective isoform.

scholarly journals Phenotypic and functional characterisation of myofibroblasts, macrophages, and lymphocytes migrating out of the human gastric lamina propria following the loss of epithelial cells

Gut ◽  
1999 ◽  
Vol 44 (3) ◽  
pp. 323-330 ◽  
Author(s):  
K C Wu ◽  
L M Jackson ◽  
A M Galvin ◽  
T Gray ◽  
C J Hawkey ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Basement Membrane ◽  
Lamina Propria ◽  
Surface Epithelium ◽  
Prostaglandin E ◽  
Tissue Samples ◽  
Membrane Pores ◽  
Functional Characterisation ◽  
Polymerase Chain ◽  
Cox 1

BACKGROUNDThe basement membrane of human colonic mucosa contains numerous discrete pores. We have recently shown that following loss of the surface epithelium, many cells migrate out of the colonic lamina propria via basement membrane pores.AIMSTo characterise cells migrating out via basement membrane pores of the human gastric lamina propria, following loss of the surface epithelium.METHODSFresh human gastric mucosal samples were completely denuded of epithelial cells and placed in culture. Tissue samples were studied by electron microscopy (EM) and cells by EM, FACS analysis, immunohistochemistry, and reverse transcription polymerase chain reaction (RT-PCR).RESULTSEM showed numerous discrete pores (0.65–8.29 μm in diameter) in the subepithelial basement membrane. During culture of mucosal samples denuded of epithelial cells, lymphocytes, macrophages, and myofibroblasts migrated out of the lamina propria via the basement membrane pores. The lymphocytes were predominantly CD45RO+ and CD69+ T cells. Macrophages were shown to express cyclooxygenase (COX) 1 and 2 enzymes. Myofibroblasts were established in culture and, despite prolonged culture and passage, retained their phenotype. They expressed mRNA and protein for COX 1 and 2 enzymes and their release of prostaglandin E2 was inhibited by selective COX 1 and 2 inhibitors.CONCLUSIONSLamina propria cells migrating out of cultured denuded gastric mucosal samples have been characterised phenotypically and functionally. Such cells would be suitable for studies of their interactions with epithelial cells and also with Helicobacter pylori and its products.

scholarly journals Effects of Nonsteroidal Anti-Inflammatory Drugs onHelicobacter pylori-Infected Gastric Mucosae of Mice: Apoptosis, Cell Proliferation, and Inflammatory Activity

2001 ◽  
Vol 69 (8) ◽  
pp. 5056-5063 ◽  
Author(s):  
Tae Il Kim ◽  
Yong Chan Lee ◽  
Kwang Hyoung Lee ◽  
Jae Ho Han ◽  
Chae Yoon Chon ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Inflammatory Activity ◽  
Prostaglandin E ◽  
Gastric Epithelial Cells ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
H Pylori ◽  
Cox 1

ABSTRACT Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are two well-known important causative factors of gastric damage. While H. pylori increases apoptosis and the proliferation of gastric epithelial cells and is an important factor in peptic ulcer and gastric cancer, NSAIDs induce cell apoptosis and have antineoplastic effects. We investigated the effects of NSAIDs (a nonselective cyclooxygenase [COX] inhibitor [indomethacin] and a selective COX-2 inhibitor [NS-398]) on the apoptosis and proliferation of gastric epithelial cells and gastric inflammation inH. pylori-infected mice. C57BL/6 mice were sacrificed 8 weeks after H. pylori SS1 inoculation. Indomethacin (2 mg/kg) or NS-398 (10 mg/kg) was administered subcutaneously once daily for 10 days before sacrifice. The following were assessed: gastric inflammatory activity, gastric COX protein expression by Western blotting; gastric prostaglandin E2 levels by enzyme immunoassay, apoptosis by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and cell proliferation by Ki67 immunostaining. Compared to the controls, H. pylori infection and/or NSAID treatment increased COX-1 and COX-2 protein expression. Gastric prostaglandin E2 levels, apoptotic index, cell proliferation index, neutrophil activity, and the degree of chronic inflammation were all increased by H. pylori infection, and these effects were significantly decreased by indomethacin treatment. However, NS-398 treatment after H. pylori infection did not induce a significant reduction, although it did result in a tendency to decrease. These results show that NSAIDs can reverse the increased apoptosis and proliferation of epithelial cells and inflammatory activity in the stomachs of H. pylori-infected mice and that, like COX-2 activation, COX-1 induction contributes to the change of gastric mucosal cell turnover and inflammation induced by H. pylori infection.

Expression of Gelatinases (MMP-2, MMP-9) and Cyclooxygenases (COX-1, COX-2) in Some Benign Salivary Gland Tumors

2012 ◽  
Vol 25 (1) ◽  
pp. 107-115 ◽  
Author(s):  
L. Lipari ◽  
A. Mauro ◽  
S. Gallina ◽  
S. Tortorici ◽  
M. Buscemi ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Salivary Gland Tumors ◽  
Benign Tumors ◽  
Chain Reaction ◽  
Quantitative Expression ◽  
Heterogenous Group ◽  
Polymerase Chain ◽  
Cox 2 ◽  
Degree Of Severity ◽  
Cox 1

Salivary gland tumors, most of which are rare benign tumors, represent a histologically heterogenous group with the greatest diversity of morphological and cellular features. The aim of this study is to analyse the expression and possible interactions between gelatinases (MMP-2, MMP-9) and cyclooxygenases (COX-1, COX-2) in some benign salivary gland tumors. We investigated the expression of gelatinases and cyclooxigenases in control salivary gland, Pleomorphic adenoma and Warthin's tumor through immunohistochemistry and Reverse Transcription – Polymerase Chain Reaction (PCR). We identified the expression of both classes of enzyme in normal samples and in the two types of pathological samples without any quantitative differences. From the present data no significant differences emerge in the expression of these enzymes among the different pathologies examined. Nevertheless, due to the small number of samples included in this study, general statements regarding correlation between the degree of severity of the tumoral pathology and the quantitative expression of these potential tumoral markers can not be made.

New Immunohistologic Findings on the Differential Role of Cyclooxygenase 1 and Cyclooxygenase 2 in Nasal Polyposis

2005 ◽  
Vol 19 (2) ◽  
pp. 111-117 ◽  
Author(s):  
Jan Gosepath ◽  
Juergen Brieger ◽  
Wolf J. Mann
Keyword(s):  
Epithelial Cells ◽  
Nasal Polyps ◽  
Nasal Polyposis ◽  
Sinus Surgery ◽  
Regulatory Function ◽  
Vascular Permeability Factor ◽  
Respiratory Mucosa ◽  
Cyclooxygenase 1 ◽  
Cox 2 ◽  
Cox 1

Background Cyclooxygenase 1 (Cox-1) plays a key role in arachidonic acid metabolism and in the pathophysiology and immunology of nasal polyposis in patients suffering from aspirin intolerance. We hypothesize that Cox-2 also might be relevant in the etiology of nasal polyps of aspirin-tolerant patients by their effects on inflammatory mediators as well as on microvascular permeability. Methods Fifty-two surgical specimens were immunohistochemically labeled for Cox-1 and Cox-2. Specimens were taken from chronically inflamed mucosa (n = 19) and from nasal polyps (n = 19) during endonasal sinus surgery. Controls were obtained from healthy nasal respiratory mucosa (n = 14), harvested during turbinate surgery in patients with nasal obstruction without inflammatory disease. Staining intensities were semiquantitatively assessed and statistically analyzed. Results In chronically inflamed tissue the expression of Cox-1 and Cox-2 was strongly labeled. However, in nasal polyps the staining pattern of Cox-1 was similar, but Cox-2 expression in epithelial cells was significantly less than in inflamed, nonpolypous specimens. Conclusion These data suggest that while Cox-1 is strongly up-regulated, Cox-2 expression is significantly lower in epithelial cells of nasal polyps than in those of chronic sinusitis without polyps. The relevance of this finding has to be discussed with respect to the regulatory function of Cox on the inflammatory reaction in nasal respiratory mucosa and its hypothetical role in alterations of capillary permeability via vascular permeability factor/vascular endothelial growth factor.

scholarly journals Effect of Interferon-τ on Prostaglandin Biosynthesis, Transport, and Signaling at the Time of Maternal Recognition of Pregnancy in Cattle: Evidence of Polycrine Actions of Prostaglandin E2

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5280-5293 ◽  
Author(s):  
J. A. Arosh ◽  
S. K. Banu ◽  
S. Kimmins ◽  
P. Chapdelaine ◽  
L. A. MacLaren ◽  
...  
Keyword(s):  
Prostaglandin F2α ◽  
Receptor Expression ◽  
Cellular Interactions ◽  
Specific Expression ◽  
Cyclooxygenase 1 ◽  
Embryonic Origin ◽  
Cox 2 ◽  
Maternal Recognition Of Pregnancy ◽  
Spatio Temporal ◽  
Cox 1

Abstract Recognition and establishment of pregnancy involve several molecular and cellular interactions among the conceptus, uterus, and corpus luteum (CL). In ruminants, interferon-τ (IFNτ) of embryonic origin is recognized as the pregnancy recognition signal. Endometrial prostaglandin F2α (PGF2α) is the luteolysin, whereas PGE2 is considered a luteoprotective or luteotrophic mediator at the time of establishment of pregnancy. The interplay between IFNτ and endometrial PGs production, transport, and signaling at the time of maternal recognition of pregnancy (MRP) is not well understood. We have studied the expression of enzymes involved in metabolism of PGE2 and PGF2α, cyclooxygenase-1 (COX-1) and COX-2, PG synthases (PGES and PGFS), PG 15-dehydrogenase, and PG transporter as well as PGE2 (EP2 and EP3) and PGF2α receptors. IFNτ influences cell-specific expression of COX-2, PGFS, EP2, and EP3 in endometrium, myometrium, and CL in a spatio-temporal and tissue-specific manner, whereas it does not alter COX-1, PGES, PG 15-dehydrogenase, PG transporter, or PGF2α receptor expression in any of these tissues. In endometrium, IFNτ decreases PGFS in epithelial cells and increases EP2 in stroma. In myometrium, IFNτ decreases PGFS and increases EP2 in smooth muscle cells. In CL, IFNτ increases PGES and decreases EP3. Together, our results show that IFNτ directly or indirectly increases PGE2 biosynthesis and EP2-associated signaling in endometrium, myometrium, and CL during MRP. Thus, PGE2 may play pivotal roles in endometrial receptivity, myometrial quiescence, and luteal maintenance, indicating polycrine (endocrine, exocrine, paracrine, and autocrine) actions of PGE2 at the time of MRP. Therefore, the establishment of pregnancy may depend not only on inhibition of endometrial PGF2α, but also on increased PGE2 production in cattle.

scholarly journals Pulmonary and Cardiorenal Cyclooxygenase-1 (COX-1), -2 (COX-2), and Microsomal Prostaglandin E Synthase-1 (mPGES-1) and -2 (mPGES-2) Expression in a Hypertension Model

2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
Zaher A. Radi ◽  
Robert Ostroski
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Cellular Localization ◽  
Vascular Endothelial Cells ◽  
Prostaglandin E ◽  
Human Hypertension ◽  
Collecting Ducts ◽  
Cox 2 ◽  
Convoluted Tubules ◽  
Cox 1

Hypertensive mice that express the human renin and angiotensinogen genes are used as a model for human hypertension because they develop hypertension secondary to increased renin-angiotensin system activity. Our study investigated the cellular localization and distribution of COX-1, COX-2, mPGES-1, and mPGES-2 in organ tissues from a mouse model of human hypertension. Male (n=15) and female (n=15) double transgenic mice (h-Ang 204/1 h-Ren 9) were used in the study. Lung, kidney, and heart tissues were obtained from mice at necropsy and fixed in 10%neutral buffered formalin followed by embedding in paraffin wax. Cut sections were stained immunohistochemically with antibodies to COX-1, COX-2, mPGES-1, and mPGES-2 and analyzed by light microscopy. Renal expression of COX-1 was the highest in the distal convoluted tubules, cortical collecting ducts, and medullary collecting ducts; while proximal convoluted tubules lacked COX-1 expression. Bronchial and bronchiolar epithelial cells, alveolar macrophages, and cardiac vascular endothelial cells also had strong COX-1 expression, with other renal, pulmonary, or cardiac microanatomic locations having mild-to-moderate expression. mPGES-2 expression was strong in the bronchial and bronchiolar epithelial cells, mild to moderate in various renal microanatomic locations, and absent in cardiac tissues. COX-2 expression was strong in the proximal and distal convoluted tubules, alveolar macrophages, and bronchial and bronchiolar epithelial cells. Marked mPGES-1 was present only in bronchial and bronchiolar epithelial cells; while mild-to-moderate expression was present in other pulmonary, renal, or cardiac microanatomic locations. Expression of these molecules was similar between males and females. Our work suggests that in hypertensive mice, there are (a) significant microanatomic variations in the pulmonary, renal, and cardiac distribution and cellular localization of COX-1, COX-2, mPGES-1, and mPGES-2, and (b) no differences in expression between genders.

Cyclooxygenase-2 is expressed in bladder during fetal development and stimulated by outlet obstruction

1997 ◽  
Vol 273 (4) ◽  
pp. F538-F544 ◽  
Author(s):  
John M. Park ◽  
Tianxin Yang ◽  
Lois J. Arend ◽  
Ann M. Smart ◽  
Jurgen B. Schnermann ◽  
...  
Keyword(s):  
Fetal Development ◽  
Outlet Obstruction ◽  
Fold Increase ◽  
Mrna Levels ◽  
Bladder Tissue ◽  
Bladder Obstruction ◽  
Bladder Distention ◽  
Polymerase Chain ◽  
Cox 2 ◽  
Cox 1

Studies were undertaken to assess expression of inducible cyclooxygenase (COX)-2 in bladder during fetal development and COX-1 and COX-2 expression after outlet obstruction. Bladder tissue or bladder progenitor tissue was harvested from CD-1 murine embryos at embryonic days 11.5( E11.5), E14.5, E17.5, E20.5 (newborn), and from adult. Bladder obstruction was created in adult female mice by ligating the urethra, and bladders were harvested after 3–24 h of obstruction. Gene expression was assessed by semiquantitative reverse transcription-polymerase chain reaction and Western blotting. COX-2 was highly expressed at the early stages of bladder development and declined progressively throughout gestation. In adult bladder, both COX-1 and COX-2 were detectable at low levels under basal conditions. An ∼30-fold increase in COX-2 mRNA was seen after 24 h of obstruction. In contrast, COX-1 did not change with obstruction. COX-2 mRNA levels peaked at 6 h of obstruction. In regional bladder-distention models, COX-2 induction was confined to the area of distention. Bladder outlet obstruction stimulates COX-2 expression dramatically, reactivating a gene that is highly expressed during fetal development.

scholarly journals Expression and localization of cyclooxygenase isoforms and cytosolic phospholipase A2 in anti-Thy-1 glomerulonephritis.

1998 ◽  
Vol 9 (3) ◽  
pp. 408-416 ◽  
Author(s):  
S Hirose ◽  
T Yamamoto ◽  
L Feng ◽  
E Yaoita ◽  
K Kawasaki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mrna Expression ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Cytosolic Phospholipase ◽  
Glomerular Epithelial Cells ◽  
Injury Model ◽  
Cox 2 ◽  
Cyclooxygenase Isoforms ◽  
Cox 1

Glomerular expression of the major rate-limiting enzymes for prostanoid synthesis, cyclooxygenase isoforms (COX-1 and COX-2) and cytosolic phospholipase A2 (cPLA2), was investigated in anti-Thy-1 nephritis in rats. Ribonuclease protection assay demonstrated minimal COX-1 mRNA expression in glomeruli of control rat kidneys and a gradual increase of expression from day 1 to day 10 after administration of monoclonal anti-rat Thy-1 antibody. On the other hand, COX-2 mRNA expression, also minimal in the normal glomeruli, was enhanced in a biphasic pattern with two peaks at 1 h and day 10. Expression of cPLA2 mRNA, which was undetectable in normal glomeruli, was induced on day 1 and increased gradually in a pattern similar to that of COX-1 mRNA expression. Immunofluorescence microscopy, using antibodies against COX isoforms, showed that both COX-1 and COX-2 were negligible or faintly detectable in the glomeruli of control rat kidneys. In contrast, the immunofluorescence for COX-1 was intensified on days 4 and 10 along the glomerular capillary walls probably in glomerular epithelial and/or endothelial cells, whereas COX-2 staining was exclusively enhanced in the glomerular epithelial cells at 1 h and day 10 during the course of anti-Thy-1 nephritis. These findings indicate that prostanoids generated through induction of COX-1, COX-2, and cPLA2 are implicated in the mediation of the mesangial cell injury model. In particular, the upregulation of COX-2 expression in glomerular epithelial cells in the selective mesangial cell injury model suggests an intercellular interaction between mesangial cells, and glomerular epithelial cells.

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