scholarly journals Differential Expression and Regulation of Microsomal Prostaglandin E2 Synthase in Human Fetal Membranes and Placenta with Infection and in Cultured Trophoblast Cells

2003 ◽  
Vol 88 (12) ◽  
pp. 6040-6047 ◽  
Author(s):  
Marina Premyslova ◽  
Wei Li ◽  
Nadia Alfaidy ◽  
Alan D. Bocking ◽  
Karen Campbell ◽  
...  
Keyword(s):  
Protein Expression ◽  
Prostaglandin E2 ◽  
Fetal Membranes ◽  
Protein Levels ◽  
Cells In Culture ◽  
Villous Trophoblast ◽  
Decidual Cells ◽  
Tnf Α ◽  
Time Of Infection ◽  
Cox 2

Abstract We have evaluated the effect of chorioamnionitis on the protein expression of microsomal and cytosolic prostaglandin E2 synthases (mPGES and cPGES) in preterm human placentae (PL) and fetal membranes (FM), by Western blot and immunohistochemistry, as well as the regulatory effect of IL-1β and TNF-α on mPGES, cPGES, and cyclooxygenase (COX)-2 expression in villous trophoblast (VT) and chorion trophoblast (CT) cell cultures. mPGES localized to the syncytiotrophoblast and vascular endothelium in PL and to the amnion epithelium, CT, and decidual cells in FM. cPGES protein was localized only to the syncytiotrophoblast in PL and had the same profile of expression as mPGES in FM. With infection, there was an increase in mPGES expression in PL and a decrease in the expression in FM. cPGES protein did not change in either PL or FM with infection. In VT cells in culture, IL-1β up-regulated COX-2 protein expression but did not affect mPGES. However, TNF-α increased both mPGES and COX-2 protein expression in these cells. In CT cells in culture, IL-1β and TNF-α increased both mPGES and COX-2 protein levels. Neither IL-1β nor TNF-α affected cPGES in either VT or CT cells. We conclude that protein levels of mPGES, as well as COX-2, can be stimulated by cytokines, potentially contributing to the increased prostaglandin production at the time of infection-driven preterm labor. However, multiple mechanisms, which apparently are inductor- and cell-type-specific, exist for the regulation of these enzymes.

scholarly journals The expression of cytokines in the milk somatic cells, blood leukocytes and serum of goats infected with small ruminant lentivirus

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Justyna Jarczak ◽  
Danuta Słoniewska ◽  
Jarosław Kaba ◽  
Emilia Bagnicka
Keyword(s):  
Protein Expression ◽  
Small Ruminant ◽  
Somatic Cells ◽  
Immunological Response ◽  
Dairy Goats ◽  
Blood Leukocytes ◽  
Protein Levels ◽  
Tnf Α ◽  
Gene And Protein Expression ◽  
Milk Somatic Cells

Abstract Background The present study aimed to determine the expression of cytokines, which is associated with the immunological response of dairy goats against small ruminant lentivirus (SRLV). The study was conducted on 26 dairy goats in their second to sixth lactation, which were divided by breed and parity into two groups: SRLV naturally infected (N = 13) and non-infected (N = 13) animals. All goats in the study were asymptomatic. The milk and blood samples, which served as studied material were taken on days 7, 30, 120 and 240 of the lactation. The gene and protein expression of several cytokines was studied using Real-Time PCR and ELISA methods. Results INF-β and INF-γ expression was down-regulated in the milk somatic cells (MSC) of SRLV-infected goats. However, an increased concentration of INF-β was observed in the MSC in SRLV-infected goats, while INF-γ expression was not observed in both SRLV-infected and non-infected animals The SRLV-infected goats also displayed decreased expression of IL-1α, IL-1β, IL-6 and INF-γ genes in the blood leukocytes,with IL-1α, IL-1β and IL-6 protein levels also being decreased in the sera. TNF-α was the only gene that demonstrated increased expression in both the MSC and the blood of infected animals; however, no such overexpression was observed at the protein level. Conclusions SRLV probably influences the immune system of infected animals by deregulating of the expression of cytokines. Further, epigenetic studies may clarify the mechanisms by which SRLV regulates the gene and protein expression of the host.

Effect of the Arctic terrestrial plant Ranunculus hyperboreus on LPS-induced inflammatory response via MAPK pathways

2018 ◽  
Vol 73 (7-8) ◽  
pp. 273-279 ◽  
Author(s):  
Chang-Suk Kong ◽  
Jung Im Lee ◽  
Fatih Karadeniz ◽  
Hojun Kim ◽  
Youngwan Seo
Keyword(s):  
Inflammatory Response ◽  
The Arctic ◽  
Mouse Macrophage ◽  
Ongoing Research ◽  
Protein Levels ◽  
Mapk Pathways ◽  
Tnf Α ◽  
Cox 2 ◽  
Bioactive Agents ◽  
Pro Inflammatory Cytokines

Abstract The Arctic flora hosts a limited number of species due to its extreme environmental conditions which also yield novel and unique secondary metabolites from withstanding plants. Considering a lack of research on bioactivity potential of Arctic flora, Ranunculus hyperboreus, an Arctic plant, was studied for its anti-inflammatory potential as a part of ongoing research on discovering novel natural bioactive products. Solvent-based fractions (H2O, n-BuOH, 85% aq. MeOH, n-hexane) from R. hyperboreus extract were observed to decrease the elevated nitrate amount during the inflammatory response of lipopolysaccharide-induced mouse macrophage RAW264.7 cells. To some extent, treatment with fractions was able to regulate the expression and protein levels of inflammation-related enzymes, iNOS and COX-2, and pro-inflammatory cytokines, TNF-α, IL-1β, and IL-6. The most active fractions, H2O and 85% aq. MeOH, were suggested to exert their effect through suppressed activation of MAPK pathways, especially JNK. Based on the studies of same species, phenolic glycosides were suggested to be the main active ingredients. To our knowledge, this is the first report of any bioactivity of R. hyperboreus which could be a valuable source of natural bioactive agents against inflammation.

Tumor necrosis factor-α stimulates gastric epithelial cell proliferation

2005 ◽  
Vol 288 (1) ◽  
pp. G32-G38 ◽  
Author(s):  
Jiing Chyuan Luo ◽  
Vivian Yvonne Shin ◽  
Ying Hua Yang ◽  
William Ka Kei Wu ◽  
Yi Ni Ye ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Mucosal Injury ◽  
Epithelial Cell Line ◽  
Epithelial Cell Proliferation ◽  
Protein Levels ◽  
Tnf Α ◽  
Cox 2 ◽  
Underlying Mechanisms ◽  
Factor Α

TNF-α is a cytokine produced during gastric mucosal injury. We examined whether TNF-α could promote mucosal repair by stimulation of epithelial cell proliferation and explored further the underlying mechanisms in a rat gastric mucosal epithelial cell line (RGM-1). TNF-α treatment (1–10 ng/ml) for 12 or 24 h significantly increased cell proliferation but did not induce apoptosis in RGM-1 cells. TNF-α treatment significantly increased cytosolic phospholipase A2 and cyclooxygenase-2 (COX-2) protein expression and PGE2 level but did not affect the protein levels of EGF, basic fibroblast growth factor, and COX-1 in RGM-1 cells. The mRNA of TNF receptor (TNF-R) 2 but not of TNF-R1 was also increased. Dexamethasone dose dependently inhibited the stimulatory effect of TNF-α on cell proliferation, which was associated with a significant decrease in cellular COX-2 expression and PGE2 level. A selective COX-2 inhibitor 3-(3-fluorophenyl)-4-[4-(methylsulfonyl)phenyl]-5,5-dimethyl-5H-furan-2-one (DFU) by itself had no effect on basal cell proliferation but significantly reduced the stimulatory effect of TNF-α on RMG-1 cells. Combination of dexamethasone and DFU did not produce an additive effect. PGE2 significantly reversed the depressive action of dexamethasone on cell proliferation. These results suggest that TNF-α plays a regulatory role in epithelial cell repair in the gastric mucosa via the TNF-α receptor and activation of the arachidonic acid/PG pathway.

scholarly journals The Influence of Interleukin (IL)-1β and IL-6 and Tumour Necrosis Factor-α on Prostaglandin Secretion from Porcine Myometrium during the First Third of Pregnancy

2010 ◽  
Vol 79 (4) ◽  
pp. 559-569 ◽  
Author(s):  
Barbara Jana ◽  
Marlena Koszykowska ◽  
Aneta Andronowska
Keyword(s):  
Protein Expression ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Uterine Contraction ◽  
Tumour Necrosis Factor Α ◽  
Cytokine Network ◽  
Tnf Α ◽  
Cox 2 ◽  
Factor Α ◽  
Necrosis Factor

The present study was undertaken to determine the effect of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) on prostaglandin (PG)F2α and PGE2 secretion as well as cyclooxygenase-2 (COX-2) protein expression in myometrium collected on days 25, 30 and 40 of pregnancy in pigs. Myometrial slices were incubated for 16 h with IL-1β, IL-6 and TNF-α (1 or 10 ng/ml of medium) or two combinations of the three cytokines (1 or 10 ng/ml of each cytokine per combination). We demonstrated the stimulatory effect of IL-1β and IL-6 on PGF2α and PGE2 secretion from myometrium collected on all examined days of pregnancy, excepting of influence of IL-6 on release of PGF2α by tissue from day 30. In turn, TNF-α was able to stimulate only PGE2 secretion by myometrium of 40-day-pregnant gilts. The three cytokines applied in combination augmented release of PGE2 from myometrium collected on days 30 and 40 of pregnancy. Stimulation of PGE2 secretion by cytokines used individually was more frequent than that of PGF2α. Moreover, an enhancement in PGF2α and/or PGE2 release was accompanied by an increase of COX-2 protein expression. Our study shows the ability of cytokines to stimulate PGF2α and PGE2 release by porcine myometrium from the first third of pregnancy. Obtained data suggest that locally PGs produced in myometrium influencing the uterine contraction activity may be important for the maintenance of myometrial quiescence during pregnancy and confirm also that the complex cytokine network is an important regulatory mechanism of PGs production during pregnancy.

scholarly journals Enhanced Cerebral Expression of MCT1 and MCT2 in a Rat Ischemia Model Occurs in Activated Microglial Cells

2009 ◽  
Vol 29 (7) ◽  
pp. 1273-1283 ◽  
Author(s):  
Tiago JTP Moreira ◽  
Karin Pierre ◽  
Fumihiko Maekawa ◽  
Cendrine Repond ◽  
Aleta Cebere ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mrna Level ◽  
Protein Levels ◽  
Microglial Cell Line ◽  
Tnf Α ◽  
Ischemic Episode ◽  
Isolectin B4 ◽  
Factor Α ◽  
Necrosis Factor

Monocarboxylate transporters (MCTs) are essential for the use of lactate, an energy substrate known to be overproduced in brain during an ischemic episode. The expression of MCT1 and MCT2 was investigated at 48 h of reperfusion from focal ischemia induced by unilateral extradural compression in Wistar rats. Increased MCT1 mRNA expression was detected in the injured cortex and hippocampus of compressed animals compared to sham controls. In the contralateral, uncompressed hemisphere, increases in MCT1 mRNA level in the cortex and MCT2 mRNA level in the hippocampus were noted. Interestingly, strong MCT1 and MCT2 protein expression was found in peri-lesional macrophages/microglia and in an isolectin B4+/S100β+ cell population in the corpus callosum. In vitro, MCT1 and MCT2 protein expression was observed in the N11 microglial cell line, whereas an enhancement of MCT1 expression by tumor necrosis factor-α (TNF-α) was shown in these cells. Modulation of MCT expression in microglia suggests that these transporters may help sustain microglial functions during recovery from focal brain ischemia. Overall, our study indicates that changes in MCT expression around and also away from the ischemic area, both at the mRNA and protein levels, are a part of the metabolic adaptations taking place in the brain after ischemia.

scholarly journals Pentahydroxy flavonoid isolated from Madhuca indica ameliorated adjuvant-induced arthritis: Possible role of TNF-α, IL’s, NF-kβ, Ikβα, COX-2, P2X7

2021 ◽  
Author(s):  
Yongliang Tang ◽  
Daotao Xie ◽  
Wenqing Gong ◽  
Hongtao Wu ◽  
Yi Qiang
Keyword(s):  
Nitrosative Stress ◽  
Autoimmune Disorder ◽  
Significant Inhibition ◽  
Withdrawal Threshold ◽  
Protein Levels ◽  
Intradermal Administration ◽  
Tnf Α ◽  
Female Wistar Rats ◽  
Cox 2

Abstract Background Rheumatoid arthritis (RA) is a chronic autoimmune disorder associated with progressive joint disability. Madhuca indica J. F. Gmel (family Sapotaceae) is an Indian medicinal plant reported to have an array of pharmacological properties. Objective To evaluate the anti-arthritic activity of isolated phytoconstituent from methanolic extract of Madhuca indica Leaves (MI-ALC) and its possible mechanism of action in FCA induced experimental arthritis. Materials and methods Polyarthritis was induced in female Wistar rats by intradermal administration of FCA (0.1 ml) into the tail. Polyarthritis was allowed to develop for the next 32 days. Then rats were treated with isolated phytoconstituent from MI-ALC (5, 10, and 20 mg/kg, p.o.) Results HPTLC, FTIR, and LC-MS spectral analysis of phytoconstituent isolated from MI-ALC confirmed the structure as 3,5,7,3′,4′- Pentahydroxy flavone (i.e., QTN). Treatment with QTN (10 and 20 mg/kg) showed significant inhibition (p < 0.05) in FCA-induced increased paw volume, joint diameter, paw withdrawal threshold, and latency. The elevated synovial oxido-nitrosative stress and protein levels of TNF-α, IL-1β, and IL-6 were significantly reduced (p < 0.05)by QTN. Western blot analysis revealed QNT significantly ameliorated (p < 0.05) up-regulated NF-kβ, Ikβα, COX-2, and P2X7 protein expressions. Conclusion QTN ameliorates FCA-induced hyperalgesia via inhibition of elevated oxido-nitrosative stress, inflammatory mediators (NF-kβ, Ikβα, COX-2, and P2X7), and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in experimental rats.

scholarly journals TNF-α potentiates lysophosphatidic acid-induced COX-2 expression via PKD in human colonic myofibroblasts

2011 ◽  
Vol 300 (4) ◽  
pp. G637-G646 ◽  
Author(s):  
Citlali Ekaterina Rodriguez Perez ◽  
Wenxian Nie ◽  
James Sinnett-Smith ◽  
Enrique Rozengurt ◽  
James Yoo
Keyword(s):  
Protein Expression ◽  
Pertussis Toxin ◽  
Lysophosphatidic Acid ◽  
Critical Role ◽  
Specific Inhibitor ◽  
Detectable Effect ◽  
Inflammatory Microenvironment ◽  
Downstream Target ◽  
Tnf Α ◽  
Cox 2

The myofibroblast (MFB) has recently been identified as an important mediator of tumor necrosis factor-α (TNF-α)-associated colitis and cancer, but the mechanism(s) involved remains incompletely understood. Here, we show that treatment of 18Co cells, a model of human colonic MFBs, with TNF-α and lysophosphatidic acid (LPA) induced striking synergistic cyclooxygenase-2 (COX-2) protein expression and production of PGE2. This effect was prevented by the LPA1 receptor antagonist Ki16425, the Giα-specific inhibitor pertussis toxin, and by the preferential protein kinase (PK) C inhibitors GF109203X and Go6983. As a known downstream target of LPA and PKC, we tested whether PKD, recently implicated in the regulation of COX-2 expression in MFB, was involved in this response. TNF-α, while having no detectable effect on the activation of PKD when added alone, augmented PKD activation stimulated by LPA, as measured by PKD autophosphorylation at Ser910. LPA-induced PKD activation was also inhibited by Ki16425, pertussis toxin, GF109203X, and Go6983. Transfection of 18Co cells with short interfering RNA targeting PKD completely inhibited the synergistic increase in COX-2 protein, demonstrating a critical role of PKD in this response. Our results imply that cross talk between TNF-α and LPA results in the amplification of COX-2 protein expression via a conserved PKD-dependent signaling pathway that appears to involve the LPA1 receptor and the G protein Giα. PKD plays a critical role in the expression of COX-2 in human colonic MFBs and may contribute to an inflammatory microenvironment that promotes tumor growth.

scholarly journals Regulation of prostaglandin production in intact fetal membranes by interleukin-1 and its receptor antagonist

1998 ◽  
Vol 159 (3) ◽  
pp. 519-526 ◽  
Author(s):  
NL Brown ◽  
SA Alvi ◽  
MG Elder ◽  
PR Bennett ◽  
MH Sullivan
Keyword(s):  
Receptor Antagonist ◽  
Partial Agonist ◽  
Interleukin 1 ◽  
Pge2 Production ◽  
Fetal Membranes ◽  
Mrna Levels ◽  
Protein Levels ◽  
Combination Treatments ◽  
Cox 2 ◽  
Cytoplasmic Phospholipase A2

There is strong evidence for the involvement of inflammatory mediators such as interleukin (IL)-1 in the biochemical mechanisms of parturition. Therefore the effects of the IL-1 family (IL-1alpha (1 ng/ml), IL-1beta (1 ng/ml) and the IL-1 receptor antagonist (IL-1ra) (10 ng/ml)) on the regulation of prostaglandin synthesis in term human fetal membranes were investigated. It was found that, after 4 h of culture, IL-1beta increased prostaglandin E2 (PGE2) output approximately twofold. This was associated with both a significant increase in cyclo-oxygenase-2 (COX-2) mRNA levels (approximately fourfold compared with control) and translocation of cytoplasmic phospholipase A2 (cPLA2) from the cytosol to the membrane fraction. IL-1alpha was less effective than IL-1beta at stimulating PGE2 production through similar mechanisms. IL-1ra had no effect on PGE2 output. However, in combination treatments, IL-1ra did not inhibit IL-1alpha- or IL-1beta-stimulated PGE2 output, and increased PGE2 production further compared with IL-1beta alone. IL-1ra decreased IL-1beta-induced COX-2 mRNA expression by about half and significantly increased cPLA2 protein levels, as detected by immunoblotting, when used alone and together with IL-1beta. These results suggest that IL-1ra has partial agonist properties when used together with IL-1alpha and IL-1beta in fetal membranes by increasing cPLA2 protein levels, which leads to an increase in the production of prostaglandins.

scholarly journals Oenanthe Javanica Extract Protects Mouse Skin from UVB Radiation via Attenuating Collagen Disruption and Inflammation

2019 ◽  
Vol 20 (6) ◽  
pp. 1435 ◽  
Author(s):  
Young Her ◽  
Bich-Na Shin ◽  
Yun Lee ◽  
Joon Park ◽  
Dae Kim ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Type Iii Collagen ◽  
Type I ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Protein Levels ◽  
Photodamaged Skin ◽  
Tnf Α ◽  
Oenanthe Javanica ◽  
Cox 2

In recent years, the use of botanical agents to prevent skin damage from solar ultraviolet (UV) irradiation has received considerable attention. Oenanthe javanica is known to exert anti-inflammatory and antioxidant activities. This study investigated photoprotective properties of an Oenanthe javanica extract (OJE) against UVB-induced skin damage in ICR mice. The extent of skin damage was evaluated in three groups: control mice with no UVB, UVB-exposed mice treated with vehicle (saline), and UVB-exposed mice treated with 1% extract. Photoprotective properties were assessed in the dorsal skin using hematoxylin and eosin staining, Masson trichrome staining, immunohistochemical staining, quantitative real-time polymerase chain reaction, and western blotting to analyze the epidermal thickness, collagen expression, and mRNA and protein levels of type I collagen, type III collagen, and interstitial collagenases, including matrix metalloproteinase (MMP)-1 and MMP-3. In addition, tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 protein levels were also assessed. In the UVB-exposed mice treated with extract, UV-induced epidermal damage was significantly ameliorated. In this group, productions of collagen types I and III were increased, and expressions of MMP-1 and MMP-3 were decreased. In addition, TNF-α and COX-2 expressions were reduced. Based on these findings, we conclude that OJE displays photoprotective effects against UVB-induced collagen disruption and inflammation and suggest that Oenanthe javanica can be used as a natural product for the treatment of photodamaged skin.

Sign in / Sign up

Export Citation Format

Share Document