scholarly journals Tumor Necrosis Factor-α Stimulates Lactate Dehydrogenase A Expression in Porcine Cultured Sertoli Cells: Mechanisms of Action

Endocrinology ◽  
1999 ◽  
Vol 140 (7) ◽  
pp. 3054-3062 ◽  
Author(s):  
Fayçal Boussouar ◽  
Renée Grataroli ◽  
Jingwei Ji ◽  
Mohamed Benahmed
Keyword(s):  
Mrna Expression ◽  
Gene Transcription ◽  
Sertoli Cells ◽  
Tumor Necrosis ◽  
Actinomycin D ◽  
Lactate Production ◽  
Mrna Levels ◽  
Kinase C ◽  
Factor Α ◽  
Necrosis Factor

Abstract In the present study, we investigated the regulatory action of tumor necrosis factor-α (TNFα) on lactate dehydrogenase A (LDH A), a key enzyme involved in lactate production. To this end, use was made of a primary culture system of porcine testicular Sertoli cells. TNFα stimulated LDH A messenger RNA (mRNA) expression in a dose (ED50 = 2.5 ng/ml; 0.1 nm TNFα)-dependent manner. This stimulatory effect was time dependent, with an effect detected after 6 h of TNFα treatment and maximal after 48 h of exposition (5-fold; P < 0.001). The direct effect of TNFα on LDH A mRNA could not be accounted for by an increase in mRNA stability (half-life = 9 h), but was probably due to an increase in LDH A gene transcription. Inhibitors of protein synthesis (cycloheximide), gene transcription (actinomycin D and dichlorobenzimidazole riboside), tyrosine kinase (genistein), and protein kinase C (bisindolylmaleimide) abrogated completely (actinomycin D, dichlorobenzimidazole riboside, cycloheximide, and genistein) or partially (bisindolylmaleimide) TNFα-induced LDH A mRNA expression. These observations suggest that the stimulatory effect of TNFα on LDH A mRNA expression requires protein synthesis and may involve a protein tyrosine kinase and protein kinase C. In addition, we report that LDH A mRNA levels were increased in Sertoli cells treated with FSH. However, although the cytokine enhances LDH A mRNA levels through increased gene transcription, the hormone exerts its stimulatory action through an increase in LDH A mRNA stability. The regulatory actions of the cytokine and the hormone on LDH A mRNA levels and therefore on lactate production may operate in the context of the metabolic cooperation between Sertoli and postmeiotic germ cells in the seminiferous tubules.

scholarly journals Alimentary induced fatty liver and adjuvant therapy with effective natural bioactive molecules

2011 ◽  
Vol 152 (26) ◽  
pp. 1035-1042 ◽  
Author(s):  
Viktor Hegedüs ◽  
Domokos Gerő ◽  
Zoltán Mihály ◽  
Attila Szijártó ◽  
Tivadar Zelles ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fatty Liver ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Redox Homeostasis ◽  
Mrna Levels ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Changes of redox-homeostasis generate cytokines, and free radicals influence many intracellular signaling pathways in different liver diseases. Liophylised table beet and carrot powder (GPS Powder Kft. 1361/004/2003BFÁÉÉÁ) containing bioactive components such as betaine, betanins, betaxanthins, flavonoids, polyphenols, glutamine, beta carotene, vitamins and folic acid may produce changes various cellular pathways. Aim: The aim of this study was to determine the protecting effects of bioactive agents of the liophylised table beet and carrot powder on fatty liver in a “short term” experiment. Method: Male Wistar rats were fed with chow with or without high fat (2% cholesterol, 0.5% cholic acid, 20% sunflower oil) and treated with 0.1 or 1 g/bwkg/day natural product for ten days parallel with the feedings. Cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-α mRNA levels were determined using molecular biologic methods. Free radicals, H-donating activity, reducing power and free SH-group concentrations were determined by luminometry and spectrophotometry. Mobilized methyl groups were assayed by over pressure liquid chromatography method in liver homogenates. Results: It was found that the higher dose of the natural product better decreased the induced free radical reactions, cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-α mRNA-levels both in normal and fatty liver tissues. Although treatments failed to exert significant changes in all global antioxidant parameters, mobilized methyl group concentrations were higher after treatments in fatty liver. Favorable tendencies were also noted in the redox-homeostasis of the fatty liver after treatment. Conclusions: As expected, lyophylised table beet and carrot proved to be a “functional food” in rats with alimentary fat induced fatty liver. It cannot be ruled out that this beneficial effect may have clinical relevance. Orv. Hetil., 2011, 152, 1035–1042.

Effect of endothelin antagonism on the production of cytokines in eosinophilic airway inflammation

2001 ◽  
Vol 280 (4) ◽  
pp. L659-L665 ◽  
Author(s):  
Finn Finsnes ◽  
Torstein Lyberg ◽  
Geir Christensen ◽  
Ole H. Skjønsberg
Keyword(s):  
Tumor Necrosis Factor ◽  
Airway Inflammation ◽  
Bronchial Asthma ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mrna Level ◽  
Mrna Levels ◽  
Proinflammatory Mediators ◽  
Factor Α ◽  
Necrosis Factor

Endothelin (ET)-1 has been launched as an important mediator in bronchial asthma, which is an eosinophilic airway inflammation. However, the interplay between ET-1 and other proinflammatory mediators during the development of airway inflammation has not been elucidated. We wanted to study 1) whether the production of ET-1 precedes the production of other proinflammatory mediators and 2) whether ET-1 stimulates the production of these mediators within the airways. These hypotheses were studied during the development of an eosinophilic airway inflammation in rats. The increase in ET-1 mRNA level in lung tissue preceded the increase in mRNA levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-8. Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-α, IL-4, IL-1β, interferon-γ, and ET-1 in bronchoalveolar lavage fluid. In conclusion, the synthesis of ET-1 as measured by increased mRNA level precedes the synthesis of other proinflammatory cytokines of importance for the development of an eosinophilic airway inflammation, and ET antagonism inhibits the production of these mediators within the airways. Whether treatment with ET antagonists will prove beneficial for patients with eosinophilic airway inflammations like bronchial asthma is not yet known.

Nocardia fractions, NLD and NWSM, induce tumor necrosis factor-α secretion in human monocytes: Role of protein kinase C

1993 ◽  
Vol 23 (7) ◽  
pp. 1582-1587 ◽  
Author(s):  
Jean Louis Mege ◽  
Thiery Jacob ◽  
Pierre Bongrand ◽  
Christian Capo ◽  
Evguenine B. Myssiakine ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Monocytes ◽  
Kinase C ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Opposing effects of tumour necrosis factor α and hyperosmolarity on Na+/myo-inositol co-transporter mRNA levels and myo-inositol accumulation by 3T3-L1 adipocytes

1998 ◽  
Vol 336 (2) ◽  
pp. 317-325 ◽  
Author(s):  
Mark A. YOREK ◽  
Joyce A. DUNLAP ◽  
William L. LOWE
Keyword(s):  
Signal Transduction ◽  
Tumour Necrosis ◽  
Actinomycin D ◽  
Signal Transduction Pathways ◽  
Mrna Levels ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Opposing Effects ◽  
Necrosis Factor

Tumour necrosis factor α (TNF-α) regulates the transport of myo-inositol in 3T3-L1 adipocytes. Treating 3T3-L1 adipocytes with TNF-α decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. TNF-α decreases the V′max for high-affinity myo-inositol transport with little change in the K′m. Studies with actinomycin D suggest that RNA synthesis is required for the TNF-α-induced effect on SMIT mRNA levels. In contrast with the effect of TNF-α, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. Hyperosmolarity increases SMIT gene expression as evidenced by the inhibition of hyperosmotic induction of SMIT mRNA levels by actinomycin D, and of myo-inositol accumulation by actinomycin D and cycloheximide. TNF-α and osmotic stress have previously been shown to activate similar signal transduction pathways in mammalian cells. In 3T3-L1 adipocytes, both TNF-α and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. TNF-α activates nuclear factor κB (NF-κB) in 3T3-L1 adipocytes but, unlike the effect of TNF-α on cultured endothelial cells, NF-κB does not seem to contribute to the regulation by TNF-α of SMIT gene expression in 3T3-L1 adipocytes. Therefore other signal transduction pathways must be considered in the regulation by TNF-α of SMIT mRNA levels and activity. Thus TNF-α and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-α might represent another mechanism by which TNF-α regulates adipocyte function.

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