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.

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.

Modulation of the prostaglandin responses of conscious rabbits to the pyrogen polyinosinic: polycytidylic acid by corticotrophin-releasing factor-41

1993 ◽  
Vol 138 (1) ◽  
pp. 7-11 ◽  
Author(s):  
N. G. N. Milton ◽  
E. W. Hillhouse ◽  
A. S. Milton
Keyword(s):  
Poly I:C ◽  
Lag Phase ◽  
Prostaglandin E ◽  
Interferon Inducer ◽  
Corticotrophin Releasing Factor ◽  
Polycytidylic Acid ◽  
Prostaglandin F ◽  
Conscious Rabbits ◽  
Polyinosinic Polycytidylic Acid

ABSTRACT The pyrogenic interferon inducer polyinosinic: polycytidylic acid (Poly I: C) was shown to stimulate rises in both prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) in conscious rabbits in vivo. Poly I:C (2·5 μg/kg) stimulated a fivefold rise in circulating immunoreactive (ir) PGE2, with a lag phase of 60 min, which was sustained during the subsequent 4-h period of observation. Poly I:C also stimulated a 2·5-fold rise in circulating irPGF2α with a lag phase of 90 min, which was followed by a return to basal levels after 5 h. The rises in circulating irPGE2 and irPGF2α stimulated by Poly I:C were prevented by pretreatment with the non-steroidal anti-inflammatory drug ketoprofen. Both the irPGE2 and irPGF2α responses to Poly I:C (2·5 μg/kg, i.v.) were antagonized by the corticotrophin-releasing factor-41 (CRF-41) receptor antagonist (α-helical CRF (9–41), 25 μg/kg, i.v.) administered 5 min prior to the pyrogen. Peripheral immunoneutralization using an anti-CRF-41 monoclonal antibody (KCHMB001, 2·5 mg/kg, i.v.) administered 5 min prior to the pyrogen, also inhibited both the PGE2 and PGF2α responses to Poly I:C (2·5 μg/kg, i.v.). However, control mouse IgG also inhibited the PGE2 response. In conclusion, these results suggest a modulatory role for endogenous peripheral CRF-41 in the circulating prostaglandin responses to the pyrogen Poly I: C and this effect may be responsible for the antipyretic actions of peripherally administered CRF-41 antagonists and antibodies. Journal of Endocrinology (1993) 138, 7–11

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 The aberrantly expressed miR-372 partly impairs sensitivity to apoptosis in parathyroid tumor cells

2018 ◽  
Vol 25 (7) ◽  
pp. 761-771 ◽  
Author(s):  
Chiara Verdelli ◽  
Irene Forno ◽  
Annamaria Morotti ◽  
Pasquale Creo ◽  
Vito Guarnieri ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Wnt Pathway ◽  
Mrna Levels ◽  
Parathyroid Tumor ◽  
Protein Levels ◽  
Parathyroid Adenomas ◽  
Tumor Parenchyma ◽  
Induced Apoptosis

Parathyroid tumors deregulate microRNAs belonging to the two clusters on the chromosome 19, the C19MC and miR-371-373 clusters. Here, we report that the embryonic miR-372 is aberrantly expressed in half of parathyroid adenomas (PAds) in most of atypical adenomas and carcinomas (n = 15). Throughin situhybridization, we identified that miR-372-positive parathyroid tumor cells were scattered throughout the tumor parenchyma. In PAd-derived cells, ectopic miR-372 inhibited the expression of its targetsCDKN1A/p21 and LATS2 at both mRNA and protein levels. Although the viability of parathyroid cells was not affected by miR-372 overexpression, the miRNA blunted camptothecin-induced apoptosis in primary PAd-derived cultures. miR-372 overexpression in parathyroid tumor cells increased parathormone (PTH) mRNA levels, and it positively correlatedin vivowith circulating PTH levels. Conversely, the parathyroid-specific genesTBX1andGCM2were not affected by miR-372 mimic transfection. Finally, miR-372 dampened the Wnt pathway in parathyroid tumor cells through DKK1 upregulation. In conclusion, miR-372 is a novel mechanism exploited by a subset of parathyroid tumor cells to partially decrease sensitivity to apoptosis, to increase PTH synthesis and to deregulate Wnt signaling.

scholarly journals The effect of acute feeding of carnitine, acetyl carnitine and propionyl carnitine on basal and A23187-stimulated eicosanoid release from rat carrageenan-elicited peritoneal macrophages

1990 ◽  
Vol 64 (2) ◽  
pp. 497-503 ◽  
Author(s):  
G. R. Elliott ◽  
A. P. M. Lauwen ◽  
I. L. Bonta
Keyword(s):  
Calcium Ionophore ◽  
Acute Effect ◽  
Peritoneal Macrophages ◽  
Calcium Ionophore A23187 ◽  
Prostaglandin E ◽  
Ionophore A23187 ◽  
Cell Functions ◽  
Prostaglandin F ◽  
Propionyl Carnitine

Little is known about the ability of carnitine to modulate cell functions. As carnitine plays an important role in lipid metabolism we investigated the acute effect of L-carnitine, L-acetyl carnitine and L-propionyl carnitine (300 mg/kg per d; 4 d) on the basal and calcium-ionophore (A23187)-stimulated release of arachidonic acid metabolites from rat carrageenan-elicited peritoneal macrophages. A decrease in the number of peritoneal carrageenan-elicited macrophages was observed after feeding all three compounds. The basal release of prostaglandin E2, 6 keto-prostaglandin F1α and leukotriene B4 was stimulated by all treatments. In contrast, thromboxane B2 production was diminished by feeding carnitine and acetyl carnitine. A23187-stimulated synthesis of 6 keto-prostaglandin F1α and leukotriene B4 was further enhanced by all three compounds. Acetyl carnitine and propionyl carnitine also enhanced thromboxane B2 synthesis. However, no effects on prostaglandin E2 formation were detected. The 6 keto-prostaglandin F1α: thromboxane B2 ratio, calculated from the basal and A23187-stimulated values, was increased by carnitine treatment. In the presence of A23187 there was also an increase in the 6 keto-prostaglandin F1α: leukotriene B4 ratio. We conclude that carnitine, and possibly some of its derivatives, could modify the macrophage component of an inflammation in vivo.

scholarly journals Syndecan-1 Amplifies Ovalbumin-Induced Airway Remodeling by Strengthening TGFβ1/Smad3 Action

2021 ◽  
Vol 12 ◽  
Author(s):  
Dong Zhang ◽  
Xin-rui Qiao ◽  
Wen-Jing Cui ◽  
Jin-tao Zhang ◽  
Yun Pan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Remodeling ◽  
Airway Epithelial Cells ◽  
Collagen I ◽  
Chronic Asthma ◽  
Airway Epithelial ◽  
Protein Levels ◽  
Rna Targeting

Syndecan-1 (SDC-1) is a transmembrane proteoglycan of heparin sulfate that can regulate various cell signal transduction pathways in the airway epithelial cells and fibroblasts. Airway epithelial cells and human bronchial fibroblasts are crucial in airway remodeling. However, the importance of SDC-1 in the remodeling of asthmatic airways has not been confirmed yet. The present study was the first to uncover SDC-1 overexpression in the airways of humans and mice with chronic asthma. This study also validated that an increase in SDC-1 expression was correlated with TGFβ1/Smad3-mediated airway remodeling in vivo and in vitro. A small interfering RNA targeting SDC-1 (SDC-1 siRNA) and homo-SDC-1 in pcDNA3.1 (pc-SDC-1) was designed to assess the effects of SDC-1 on TGFβ1/Smad3-mediated collagen I expression in Beas-2B (airway epithelial cells) and HLF-1 (fibroblasts) cells. Downregulation of the SDC-1 expression by SDC-1 siRNA remarkably attenuated TGFβ1-induced p-Smad3 levels and collagen I expression in Beas-2B and HLF-1 cells. In addition, SDC-1 overexpression with pc-SDC-1 enhanced TGFβ1-induced p-Smad3 level and collagen I expression in Beas-2B and HLF-1 cells. Furthermore, the levels of p-Smad3 and collagen I induced by TGFβ1 were slightly increased after the addition of the recombinant human SDC-1 protein to Beas-2B and HLF-1 cells. These findings in vitro were also confirmed in a mouse model. A short hairpin RNA targeting SDC-1 (SDC-1 shRNA) to interfere with SDC-1 expression considerably reduced the levels of p-Smad3 and remodeling protein (α-SMA, collagen I) in the airways induced by ovalbumin (OVA). Similarly, OVA-induced p-Smad3 and remodeling protein levels in airways increased after mice inhalation with the recombinant mouse SDC-1 protein. These results suggested that SDC-1 of airway epithelial cells and fibroblasts plays a key role in the development of airway remodeling in OVA-induced chronic asthma.

Endometrial prostaglandins and menorrhagia: influence of a prostaglandin synthetase inhibitor in vivo

1987 ◽  
Vol 65 (10) ◽  
pp. 2081-2084 ◽  
Author(s):  
B. K. Tsang ◽  
M. T. Domingo ◽  
J. E. H. Spence ◽  
P. R. Garner ◽  
D. K. Dudley ◽  
...  
Keyword(s):  
Blood Loss ◽  
Mefenamic Acid ◽  
Menstrual Blood ◽  
Etiologic Factor ◽  
Prostaglandin E ◽  
Menstrual Blood Loss ◽  
Prostaglandin Synthetase ◽  
Double Blind ◽  
Prostaglandin F

Prostaglandin levels in the human endometrium were determined on day 2 of the menstrual cycle in eumenorrheic subjects and in patients with menorrhagia, dysmenorrhea, or both. Menorrhagic subjects had significantly higher levels of endometrial prostaglandins of the E and F series when compared with eumenorrheics. Prostaglandin E levels were markedly higher than prostaglandin F. In 10 menorrhagic subjects who completed a double-blind clinical study on the effectiveness of mefenamic acid in lowering menstrual blood loss, 9 exhibited statistically significant reduction in endometrial prostaglandin levels. A decrease in menstrual blood loss was also noted during mefenamic acid treatment in these patients. These findings are consistent with the concept that abnormally high uterine prostaglandin levels may be an important etiologic factor in menorrhagia and support the notion that one of the mechanisms of action of nonsteroidal anti-inflammatory agents in the treatment of this menstrual disorder is inhibition of endometrial prostaglandin production.

TGF-α reduces bradykinin-stimulated ion transport and prostaglandin release in human colonic epithelial cells

1999 ◽  
Vol 276 (4) ◽  
pp. C848-C855 ◽  
Author(s):  
J. Beltinger ◽  
C. J. Hawkey ◽  
W. A. Stack
Keyword(s):  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Prostaglandin E ◽  
Intracellular Camp ◽  
Colonic Epithelial Cells ◽  
Transforming Growth Factor Α ◽  
Prostaglandin Release

The effect of chronic exposure to transforming growth factor-α (TGF-α) on bradykinin-stimulated acute prostanoid production and ion secretion in monolayers of HCA-7 colony 29 colonic epithelial cells has been studied. Monolayers synthesized prostaglandin E2(PGE2) at a basal rate of 2.10 ± 0.31 pg ⋅ monolayer−1 ⋅ min−1over 24 h. Bradykinin (10−8–10−5M) dose dependently increased acute PGE2 release by three orders of magnitude. This was associated with a rise in cAMP from 1.60 ± 0.14 to 2.90 ± 0.1 pmol/monolayer ( P < 0.02) and a dose-dependent increase in short-circuit current (SCC). When monolayers were primed by a 24-h exposure to TGF-α, basal PGE2 release rose to 6.31 ± 0.38 pg ⋅ monolayer−1 ⋅ min−1(TGF-α concn 10 ng/ml; P = 0.001). However, the stimulation of acute prostaglandin release, intracellular cAMP, and increased SCC by bradykinin was significantly reduced by preincubation with TGF-α. Priming with PGE2(10−8–10−6M) over 24 h mimicked the effect of TGF-α on bradykinin-induced changes in cAMP and SCC. These data suggest that enhanced chronic release of prostaglandins in response to stimulation with TGF-α may downregulate acute responses to bradykinin. In vivo, TGF-α could have an important modulatory function in regulating secretion under inflammatory conditions.

scholarly journals Immunohistochemical profile of HIF-1α, VEGF-A, VEGFR2 and MMP9 proteins in tegumentary leishmaniasis

2012 ◽  
Vol 87 (5) ◽  
pp. 709-713 ◽  
Author(s):  
Carlos Alberto de Carvalho Fraga ◽  
Marcos Vinicius Macedo de Oliveira ◽  
Lucas Rodrigues Alves ◽  
Agostinho Gonçalves Viana ◽  
Adriana Alkmin de Sousa ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Skin Lesions ◽  
Activation Mechanism ◽  
In Vivo Studies ◽  
Protein Levels ◽  
Tegumentary Leishmaniasis ◽  
Protein Expressions

BACKGROUND: Leishmaniasis is one of the most important infectious diseases worldwide. Our study can provide more knowledge about angiogenic and hypoxic events in leishmaniasis. We attempted to verify whether the HIF-1 α protein expression may be associated to VEGF-A, VEGFR2 and MMP9 in leishmanial lesions. OBJECTIVES: Besides understanding the pathway, we performed the correlation of VEGF-A, VEGFR2 and MMP9 proteins. METHODS: In this study, we gathered 54 paraffin blocks taken from skin lesions in patients from northern Minas Gerais, Brazil, with confirmed diagnosis of tegumentary leishmaniasis. Immunohistochemistry was used to evaluate the expression of the proteins. The expression of HIF-1α was categorized into two groups according to the median: HIF-1 α lower and HIF-1 α higher. RESULTS: We observed increase of VEGFR2 and MMP9 protein expressions in HIF-1 α higher group of epithelial cells. Spearman analyses in epithelial cells showed correlation between VEGF-A and MMP9, VEGFR2 and MMP9 protein expression. CONCLUSIONS: HIF-1 α higher group showed increase of VEGFR2 and MMP9 proteins. In epithelial cells, VEGF-A was correlated to MMP9 protein. Furthermore, considering leukocyte cells, VEGFR2 was negatively correlated to MMP9 protein levels. This pathway possibly prepares the cells for a higher activity in a hypoxic or an angiogenic microenvironment. Other in vitro and in vivo studies may clarify the activation mechanism and the response from the proteins HIF-1 α, VEGFR2 and MMP-9 in tegumentary leishmaniasis.

Polyamine-mediated reduction in human airway epithelial migration in response to wounding is PGE2dependent through decreases in COX-2 and cPLA2protein levels

2006 ◽  
Vol 101 (4) ◽  
pp. 1127-1135 ◽  
Author(s):  
Mark J. Cowan ◽  
Timothy Coll ◽  
James H. Shelhamer
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Cyclooxygenase 2 ◽  
Phospholipase A ◽  
Prostaglandin E ◽  
Airway Epithelial ◽  
Cyclooxygenase Inhibition ◽  
Protein Levels ◽  
Human Airway ◽  
Cytosolic Phospholipase

Both ornithine decarboxylase inhibition to deplete polyamines and cyclooxygenase inhibition diminish the migration response to injury of human airway epithelial cells in tissue culture monolayers by ∼75%. Restoration of normal migration responses is achieved in the polyamine depleted system either by exogenous reconstitution of polyamines or the addition of prostaglandin E2(PGE2). However, only PGE2was able to restore migration in the cyclooxygenase-inhibited systems. Western blot for cyclooxygenase-2 and cytosolic phospholipase A2protein levels and ELISAs for PGE2secretion demonstrate dramatic increases over 24–48 h after monolayer wounding. These increases are completely abolished by polyamine depletion or cyclooxygenase inhibition. We conclude that polyamine inhibition decreases cellular migration in response to injury in airway epithelial cells at least in part through inhibiting normal PGE2production in response to injury. This may be brought about by decreases in cytosolic phospholipase A2and cyclooxygenase-2 protein levels.

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