scholarly journals The prostaglandin E2 receptor PTGER2 and prostaglandin F2α receptor PTGFR mediate oviductal glycoprotein 1 expression in bovine oviductal epithelial cells

2018 ◽  
Vol 64 (2) ◽  
pp. 101-108
Author(s):  
Nan ZHANG ◽  
Wei MAO ◽  
Ying ZHANG ◽  
Na HUANG ◽  
Bo LIU ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Prostaglandin E ◽  
Prostaglandin F

scholarly journals Polarised bovine endometrial epithelial cells vectorially secrete prostaglandins and chemotactic factors under physiological and pathological conditions

Reproduction ◽  
2013 ◽  
Vol 145 (1) ◽  
pp. 57-72 ◽  
Author(s):  
Siân B MacKintosh ◽  
Hans-Joachim Schuberth ◽  
Laura L Healy ◽  
I Martin Sheldon
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Bacterial Infection ◽  
Stromal Cells ◽  
Neutrophil Migration ◽  
Response To Treatment ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Chemotactic Factors ◽  
Endometrial Epithelial Cells

Epithelial cells of the endometrium secrete prostaglandins to regulate the bovine oestrous cycle and form a functional barrier to microbes. However, bacterial infection of the endometrium commonly causes infertility in dairy cattle by disrupting endometrial physiology. Epithelial cell cultures are used to study the mechanisms of physiology and pathology, but 2D cultures may not reflect the 3D complexity of the epithelium. In this study, a polarised epithelial cell transwell culture was developed, using transepithelial resistance (TER), to monitor epithelial integrity. Polarised epithelial cells were treated with oxytocin and arachidonic acid to test physiological function and with lipopolysaccharide (LPS) to mimic bacterial infection. Supernatants were analysed for prostaglandin E2(PGE), prostaglandin F2α, the chemokine interleukin-8 (IL8) and the ability of supernatants to induce neutrophil migration. Confluent epithelial cells established polarity when TER was >1800 Ωcm2and predominantly released prostaglandins basolaterally. In contrast, IL8 from epithelial cells accumulated apically and the supernatants were highly chemotactic for neutrophils. The striking exception was when the epithelial cells were treated with LPS in the apical or basolateral compartment independently, which led to the release of IL8 towards the treated compartment. Although stromal cells also accumulated PGE and IL8 in response to treatment, co-culture of stromal cells in the well below polarised epithelial cells did not influence cellular responses. In conclusion, polarised endometrial epithelial cells vectorially released prostaglandins and chemokines to reflect their respective mechanistic roles in physiology and pathology.

scholarly journals Regulation of the prostaglandin enzymatic system by estradiol and progesterone in nonpregnant sheep cervix

Reproduction ◽  
2007 ◽  
Vol 133 (5) ◽  
pp. 1027-1034 ◽  
Author(s):  
Qi Zhang ◽  
Valta Collins ◽  
Kaushik Chakrabarty ◽  
James C Rose ◽  
Wen Xuan Wu
Keyword(s):  
Epithelial Cells ◽  
Prostaglandin E ◽  
Enzymatic System ◽  
Sheep Model ◽  
Protein Levels ◽  
Progesterone Treatment ◽  
Potent Stimulator ◽  
Prostaglandin F

In the present study, we examined thein vivoeffects of estradiol (E2) and progesterone on cyclooxygenase (COX) 2, prostaglandin F synthase (PTGFS, also known as PGFS), and membrane-associated prostaglandin E synthase 1 (mPTGES1) expression at both mRNA and protein levels using a nonpregnant ovariectomized (OVX) sheep model. Sixteen ewes were OVX shortly after ovulation. After 40 days, ewes were treated with saline (Cont,n=5), or E2infused intravenously for 2 days (50 μg/day,n=5) or intravaginal progesterone (P) sponges for 10 days (0.3 g P,n=6). Cervical COX2, PTGFS, and mPTGES1 mRNA and protein were quantified by northern and western blot analyses respectively.In situhybridization and/or immunocytochemistry were used to localize the cellular distribution of COX2, PTGFS, and mPTGES1 mRNAs and proteins. COX2 mRNA abundance increased significantly in the cervix after E2treatment (P<0.05). However, progesterone was a more potent stimulator than E2of COX2 mRNA and protein abundance in the cervix (P<0.01). In contrast, PTGFS and mPTGES1 mRNA and protein concentrations did not change after E2or progesterone treatment (P>0.05). COX2, PTGFS, and mPTGES1 mRNA and protein were only localized in cervical glandular epithelial cells. This study shows that increased cervical COX2 mRNA and protein, but not PTGFS and mPTGES1 mRNA and protein, were associated with E2and progesterone treatment in nonpregnant sheep. More strikingly, progesterone was a more potent stimulator of cervical COX2 expression than E2. The expression of COX2, PTGFS, and mPTGES1 mRNA and/or protein was confined in the cervical glandular epithelial cells of nonpregnant sheep.

scholarly journals Accumulation of Prostacyclin in Rat Brain during Haemorrhagic Hypotension—Possible Role of PGI2 in Autoregulation

1984 ◽  
Vol 4 (1) ◽  
pp. 107-109 ◽  
Author(s):  
E. Shohami ◽  
A. Sidi
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Control Group ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Arterial Blood ◽  
Haemorrhagic Hypotension ◽  
Potent Vasodilator ◽  
Prostaglandin F

The effect of haemorrhagic hypotension on the levels of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto prostaglandin F1α (6-keto-PGF1α) in cortical tissue of rats was studied. Lightly anesthetized rats were subjected to steady-state hypotension for 15 min, with a mean arterial blood pressure of 80, 60, and 40 mm Hg, and compared to a control group of normotensive rats. No significant change was found in the levels of PGE2 and TXB2. The level of 6-keto-PGF1α increased from 7.8 ± 0.9 to 14.1 ± 1.9 pg/mg protein (p < 0.02) at 80 mm Hg. Our findings suggest that prostacyclin, which is a potent vasodilator, might play a role in setting the lower limit of the autoregulation range.

Pro-inflammatory and vasoconstricting prostanoid PGF2α causes no headache in man

Cephalalgia ◽  
2011 ◽  
Vol 31 (15) ◽  
pp. 1532-1541 ◽  
Author(s):  
Maria Antonova ◽  
Troels Wienecke ◽  
Jes Olesen ◽  
Messoud Ashina
Keyword(s):  
Healthy Volunteers ◽  
Rating Scale ◽  
Superficial Temporal Artery ◽  
Area Under The Curve ◽  
Temporal Artery ◽  
Human Model ◽  
Prostaglandin E ◽  
Signalling Molecules ◽  
Prostaglandin F

Background: During two decades of migraine provocation studies with naturally occurring signalling molecules, vasodilators such as prostaglandin E2, prostaglandin I2 (prostacyclin) and prostaglandin D2 were shown to be able to induce headache in man. To elucidate the role of inflammation and vasodilatation in the generation of headache, we investigated whether the pro-inflammatory and vasoconstricting prostanoid prostaglandin F2α (PGF2α) would cause headache in a human model of headache. Methods: Twelve healthy volunteers were randomly allocated to receive 3.5 µg/kg/min PGF2α or placebo over 20 min in a two-way crossover study. We recorded headache intensity on a verbal rating scale, middle cerebral artery blood flow velocity (VMCA) and the diameters of the superficial temporal artery (STA) and radial artery (RA). Results: We found no difference in the area under the curve (AUC) for immediate headache (0–90 min) between PGF2α and placebo ( p = 0.144). The McNemar's test showed no difference in the incidence of immediate and delayed headache between verum and placebo ( p = 0.500 and p = 1.000, respectively). There was no difference in VMCA ( p = 0.776) and in the diameter of the STA ( p = 0.460) or RA ( p = 0.780) between PGF2α and placebo. Conclusion: The present study shows that PGF2α, unlike vasodilating prostaglandins, does not provoke headache. We suggest that the vasodilating abilities of prostaglandins are important for the induction of experimental headache in healthy volunteers.

PRODUCTION OF PROSTAGLANDINS BY THE GUINEA-PIG UTERUS

1972 ◽  
Vol 54 (1) ◽  
pp. 147-159 ◽  
Author(s):  
N. L. POYSER
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Oestrous Cycle ◽  
Prostaglandin E ◽  
Prostaglandin F

SUMMARY The production of prostaglandins by the uterus and the resting levels of prostaglandins in the uterus on selected days of the oestrous cycle were determined in guinea-pigs. Prostaglandin F2α was detectable in the guinea-pig uterus in small amounts on days 13, 14 and 15 of the cycle. Prostaglandin E2 was present in even smaller amounts on days 14 and 15. The homogenized guinea-pig uterus had the ability to biosynthesize prostaglandins, from endogenous precursors, during incubation on every day of the cycle studied. Four to six times more prostaglandin F2α than E2 was produced on any one day with the amounts of prostaglandins formed increasing towards the end of the oestrous cycle. Indomethacin inhibited the biosynthesis of prostaglandins by the guinea-pig uterus. The implications of these findings are discussed.

scholarly journals NSAID-induced injury of gastric epithelial cells is reversible: roles of mitochondria, AMP kinase, NGF, and PGE2

2019 ◽  
Vol 317 (6) ◽  
pp. G862-G871
Author(s):  
Amrita Ahluwalia ◽  
Neil Hoa ◽  
Michael K. Jones ◽  
Andrzej S. Tarnawski
Keyword(s):  
Membrane Potential ◽  
Nerve Growth Factor ◽  
Epithelial Cells ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cell Injury ◽  
Prostaglandin E ◽  
Gastric Epithelial Cells ◽  
Amp Kinase

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DFN) and indomethacin (INDO) are extensively used worldwide. Their main side effects are injury of the gastrointestinal tract, including erosions, ulcers, and bleeding. Since gastric epithelial cells (GEPCs) are crucial for mucosal defense and are the major target of injury, we examined the extent to which DFN- and INDO-induced GEPC injury can be reversed by nerve growth factor (NGF), 16,16 dimethyl prostaglandin E2 (dmPGE2), and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), the pharmacological activator of the metabolic sensor AMP kinase (AMPK). Cultured normal rat gastric mucosal epithelial (RGM1) cells were treated with PBS (control), NGF, dmPGE2, AICAR, and/or NSAID (DFN or INDO) for 1–4 h. We examined cell injury by confocal microscopy, cell death/survival using calcein AM, mitochondrial membrane potential using MitoTracker, and phosphorylation of AMPK by Western blotting. DFN and INDO treatment of RGM1 cells for 2 h decreased mitochondrial membrane potential and cell viability. NGF posttreatment (initiated 1 or 2 h after DFN or INDO) reversed the dissipation of mitochondrial membrane potential and cell injury caused by DFN and INDO and increased cell viability versus cells treated for 4 h with NSAID alone. Pretreatment with dmPGE2 and AICAR significantly protected these cells from DFN- and INDO-induced injury, whereas dmPGE2 and AICAR posttreatment (initiated 1 h after NSAID treatment) reversed cell injury and significantly increased cell viability and rescued the cells from NSAID-induced mitochondrial membrane potential reduction. DFN and INDO induce extensive mitochondrial injury and GEPC death, which can be significantly reversed by NGF, dmPGE2, and AICAR. NEW & NOTEWORTHY This study demonstrated that mitochondria are key targets of diclofenac- and indomethacin-induced injury of gastric epithelial cells and that diclofenac and indomethacin injury can be prevented and, importantly, also reversed by treatment with nerve growth factor, 16,16 dimethyl prostaglandin E2, and 5-aminoimidazole-4-carboxamide ribonucleotide.

Cellular localization of mRNAs for prostaglandin E receptor subtypes in mouse gastrointestinal tract

1997 ◽  
Vol 272 (3) ◽  
pp. G681-G687 ◽  
Author(s):  
K. Morimoto ◽  
Y. Sugimoto ◽  
M. Katsuyama ◽  
H. Oida ◽  
K. Tsuboi ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Epithelial Cells ◽  
Cellular Localization ◽  
The Body ◽  
Prostaglandin E ◽  
Receptor Subtypes ◽  
Fundic Gland ◽  
Intestinal Functions ◽  
Myenteric Ganglia

Regional and cellular distribution of mRNAs for prostaglandin E (PGE) receptor subtypes was investigated in the mouse gastrointestinal tract by in situ hybridization. Strong signals for EP1 transcripts were detected in cells of the muscularis mucosae layer, especially in the body of the stomach. Intense signals for EP3 transcripts were detected in neurons of the myenteric ganglia throughout the tract. Moderate EP3 mRNA expression was also observed in fundic gland epithelial cells, except for surface mucous cells in the stomach. Expression of EP4 mRNA was moderate in surface epithelial cells of the corpus and in glands from the surface to the base of the antrum. Strong EP4 signals were observed in the epithelium in the duodenum, jejunum, and ileum. In the ileum, signals were only observed in the upper part of the villi. However, no or weak signals for EP2 transcripts were detected. These findings suggest that PGE2 modulates various gastric or intestinal functions via at least three different PGE receptors.

Urinary Excretion and Glomerular Synthesis of Prostaglandin E2 and Prostaglandin F2α in Cirrhotic, Non-Ascitic Rats: The Effects of Sodium Overload

Nephron ◽  
1988 ◽  
Vol 49 (4) ◽  
pp. 322-327 ◽  
Author(s):  
Juan Carlos Santos ◽  
Diego Rodríguez-Puyol ◽  
Alicia Blanchart ◽  
Luis Hernando ◽  
José Miguel López-Novoa
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Sodium Overload

Role of interleukin-1β in the regulation of porcine corpora lutea during the late luteal phase of the cycle and during pregnancy

2012 ◽  
Vol 60 (3) ◽  
pp. 395-407 ◽  
Author(s):  
Agata Zmijewska ◽  
Anita Franczak ◽  
Genowefa Kotwica
Keyword(s):  
Secretory Activity ◽  
Oestrous Cycle ◽  
Interleukin 1Β ◽  
Prostaglandin E ◽  
Corpora Lutea ◽  
Prostaglandin Synthase ◽  
Late Luteal Phase ◽  
Prostaglandin F ◽  
Hormonal Milieu

Interleukin-1β (IL-1β) may regulate ovarian physiology. In this study, the influence of IL-1β on secretory activity within the corpora lutea (CL) of cyclic and gravid pigs was determinedin vitroduring different stages of the CL lifespan, e.g. on Days 10–11, 12–13 and 15–16 of the oestrous cycle and pregnancy. IL-1β (10 ng/ml) increased prostaglandin E2(PGE2) secretion from CL of the cyclic and gravid pigs during studied days of the oestrous cycle and pregnancy. Increase (P < 0.05) of prostaglandin F2α(PGF2α) in IL-1β-treated CL was demonstrated only on Days 10–11 of the oestrous cycle. More potent stimulatory effect of IL-1β on PGE2than PGF2αsecretion resulted in the enhancement of the PGE2:PGF2αratio in cyclic and early pregnant CL. IL-1β increased (P < 0.05) progesterone (P4) secretion only in gravid CL and had no effect on oestradiol-17β (E2) release. Expression of cyclooxygenase-2 (COX-2) mRNA was stimulated (P < 0.05) in IL-1β-treated cyclic and gravid CL. Expression of prostaglandin synthase mRNAs in response to IL-1β did not increase. In conclusion, IL-1β modulates PGE2, PGF2αand P4secretion from porcine CL, depending on luteal stage and the surrounding hormonal milieu. The cytokine may act locally in porcine CL for luteotrophic support throughout the PGE2-mediated synthesis and secretion.

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