scholarly journals Turnour necrosis factor stimulates endothelin-1 gene expression in cultured bovine endothelial cells

1992 ◽  
Vol 1 (4) ◽  
pp. 263-266 ◽  
Author(s):  
Silvia Orisio ◽  
Marina Morigi ◽  
Carla Zoja ◽  
Norberto Perico ◽  
Giuseppe Remuzzi
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Hypotensive Effect ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Endothelin 1 ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We have studied the effect of human recombinant tumour necrosis factor-α (TNF-α) on gene expression and production of endothelin-1 in cultured bovine aortic endothelial cells. TNF-α (10 and 100 ng ml−1) increased in a time dependent manner the preproendothelin-1 mRNA levels in respect to unstimulated endothelial cells. TNF-α induced endothelin-1 gene expression was associated with a parallel increase in the release of the corresponding peptide in the culture medium. These findings suggest that the enhanced synthesis and release of endothelin-1 occurring in conditions of increased generation of TNF, may act as a modulatory factor that counteracts the hypotensive effect and the excessive platelet aggregation and adhesion induced by TNF.

Tumour necrosis factor-α gene expression and production in human umbilical arterial endothelial cells

2000 ◽  
Vol 98 (4) ◽  
pp. 461-470 ◽  
Author(s):  
Thomas NEUHAUS ◽  
Gudrun TOTZKE ◽  
Elisabeth GRUENEWALD ◽  
Hans-Peter JUESTEN ◽  
Agapios SACHINIDIS ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Dependent Manner ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Arterial Endothelial Cells ◽  
Necrosis Factor

Endothelial cells act as an interface between the blood and tissues, and are known to be involved in inflammatory processes. These cells are responsive to and produce different cytokines. Tumour necrosis factor-α (TNF-α) not only is one of the most important inflammatory peptides, but also can be induced by lipopolysaccharide (LPS). The focus of the present study was on TNF-α gene expression and production in human umbilical arterial endothelial cells (HUAEC), including the kinetics of this process. Interleukin-1α (IL-1α), LPS and TNF-α, which are all known to be elevated in septic shock, were used as stimulators at concentrations commonly found in patients with sepsis. Through the use of reverse transcriptase/PCR, immunohistochemical reactions and ELISA techniques, we showed that, in HUAEC, all three stimuli were able to induce gene expression and production of TNF-α. Furthermore, this induction by IL-1α, LPS and TNF-α occurred in a time- and concentration-dependent manner in these cells. TNF-α expression and production was induced by all three agents at concentrations commonly found in patients with sepsis. TNF-α mRNA was observed within 30 min regardless of the stimulus used, but the levels peaked at different times. Since it is well established that TNF-α is able to induce the synthesis of IL-1α in endothelial cells and, as shown in the present study, TNF-α and IL-1α are themselves able to induce the synthesis of TNF-α in endothelial cells, an autocrine potentiation of cytokine release in sepsis can be proposed. This situation could lead to a locally acting ‘vicious cycle’ which, when considered in addition to the known ability of TNF-α to induce apoptosis, could mean that various organs will be damaged, a condition associated with sepsis. Thus these results provide further evidence for the important role played by the endothelium in inflammation.

Effect of TNF-α on SMIT mRNA levels andmyo-inositol accumulation in cultured endothelial cells

1998 ◽  
Vol 274 (1) ◽  
pp. C58-C71 ◽  
Author(s):  
Mark A. Yorek ◽  
Joyce A. Dunlap ◽  
Michael J. Thomas ◽  
Patrick R. Cammarata ◽  
Cheng Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Mrna Levels ◽  
Kinase C ◽  
Cultured Endothelial Cells ◽  
Tnf Α ◽  
Protein Kinase C Inhibitor ◽  
Factor Α ◽  
Necrosis Factor ◽  
Cerebral Microvessel

Previously we have shown that hyperosmolarity increases Na+- myo-inositol cotransporter (SMIT) activity and mRNA levels in cultured endothelial cells. Because hyperosmolarity and cytokines, such as tumor necrosis factor-α (TNF-α), activate similar signal transduction pathways, we examined the effect of TNF-α on SMIT mRNA levels and myo-inositol accumulation. In contrast to the effect of hyperosmolarity, TNF-α caused a time- and concentration-dependent decrease in SMIT mRNA levels and myo-inositol accumulation. The effect of TNF-α on myo-inositol accumulation was found in large-vessel endothelial cells (derived from the aorta and pulmonary artery) and cerebral microvessel endothelial cells. In bovine aorta and bovine pulmonary artery endothelial cells, TNF-α activated nuclear factor (NF)-κB. TNF-α also increased ceramide levels, and C2-ceramide mimicked the effect of TNF-α on SMIT mRNA levels and myo-inositol accumulation in bovine aorta endothelial cells. Pyrrolidinedithiocarbamate, genistein, and 7-amino-1-chloro-3-tosylamido-2-hepatanone, compounds that can inhibit NF-κB activation, partially prevented the TNF-α-induced decrease in myo-inositol accumulation. The effect of TNF-α on myo-inositol accumulation was also partially prevented by the protein kinase C inhibitor calphostin C but not by staurosporine. These studies demonstrate that TNF-α causes a decrease in SMIT mRNA levels and myo-inositol accumulation in cultured endothelial cells, which may be related to the activation of NF-κB.

scholarly journals Delivering Minocycline into Brain Endothelial Cells with Liposome-Based Technology

2012 ◽  
Vol 32 (6) ◽  
pp. 983-988 ◽  
Author(s):  
Changhong Xing ◽  
Tatyana Levchenko ◽  
Shuzhen Guo ◽  
Monique Stins ◽  
Vladimir P Torchilin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis ◽  
Proof Of Concept ◽  
Brain Endothelial Cells ◽  
Cerebral Endothelium ◽  
Low Concentrations ◽  
Tnf Α ◽  
Factor Α ◽  
Very High ◽  
Necrosis Factor

Minocycline has been proposed as a way to blunt neurovascular injury from matrix metalloproteinases (MMPs) during stroke. However, recent clinical trials suggest that high levels of minocycline may have deleterious side-effects. Here, we showed that very high minocycline concentrations damage endothelial cells via calpain/caspase pathways. To alleviate this potential cytotoxicity, we encapsulated minocycline in liposomes. Low concentrations of minocycline could not reduce tumor necrosis factor α (TNF α)-induced MMP-9 release from endothelial cells. But low concentrations of minocycline-loaded liposomes significantly reduced TNF α-induced MMP-9 release. This study provides proof-of-concept that liposomes may be used to deliver lower levels of minocycline for targeting MMPs in cerebral endothelium.

Epigallocatechin Gallate Modulates Cytokine Production by Bone Marrow-Derived Dendritic Cells Stimulated with Lipopolysaccharide or Muramyldipeptide, or Infected with Legionella pneumophila

2005 ◽  
Vol 230 (9) ◽  
pp. 645-651 ◽  
Author(s):  
James Rogers ◽  
Izabella Perkins ◽  
Alberto van Olphen ◽  
Nicholas Burdash ◽  
Thomas W. Klein ◽  
...  
Keyword(s):  
Legionella Pneumophila ◽  
Tumor Necrosis ◽  
Epigallocatechin Gallate ◽  
Dependent Manner ◽  
Enhanced Production ◽  
Tnf Α ◽  
Factor Α ◽  
Dose Dependent ◽  
Antimicrobial Immunity ◽  
Necrosis Factor

The primary polyphenol in green tea extract is the catechin epigallocatechin gallate (EGCG). Various studies have shown significant suppressive effects of catechin on mammalian cells, either tumor or normal cells, including lymphoid cells. Previous studies from this laboratory reported that EGCG has marked suppressive activity on murine macrophages infected with the intracellular bacterium Legionella pneumophila (Lp), an effect mediated by enhanced production of both tumor necrosis factor-α (TNF-α) and γ-interferon (IFN-γ). In the present study, primary murine bone marrow (BM)-derived dendritic cells (DCs), a phagocytic monocytic cell essential for innate immunity to intracellular microorganisms, such as Lp, were stimulated in vitro with the microbial stimulant lipopolysaccharide (LPS) from gram-negative bacteria, the cell wall component from gram-positive bacteria muramyldipeptide (MDP) or infected with Lp. Production of the T helper cell (Th1)-activating cytokine, interleukin-12 (IL-12) and the proinflammatory cytokine, tumor necrosis factor-α (TNF-α), produced mainly by phagocytic cells and important for antimicrobial immunity, was determined in cell culture supernatants by enzyme-linked immunosorbent assay (ELISA). Treatment of the cells with EGCG inhibited, in a dose-dependent manner, production of IL-12. In contrast, enhanced production of TNF-α occurred in a dose-dependent manner in the DC cultures stimulated with either soluble bacterial product or infected with Lp. Thus, the results of this study show that the EGCG catechin has a marked effect in modulating production of these immunoregulatory cytokines in stimulated DCs, which are important for antimicrobial immunity, especially innate immunity. Further studies are necessary to characterize the physiologic function of the effect of EGCG on TNF-α and IL-12 during Lp infection, and the mechanisms involved.

In VitroProtective Effects of Two Extracts from Bergamot Peels on Human Endothelial Cells Exposed to Tumor Necrosis Factor-α (TNF-α)

2010 ◽  
Vol 58 (14) ◽  
pp. 8430-8436 ◽  
Author(s):  
Domenico Trombetta ◽  
Francesco Cimino ◽  
Mariateresa Cristani ◽  
Giuseppina Mandalari ◽  
Antonella Saija ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Endothelial Cells ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Role of α2-macroglobulin in fever and cytokine responses induced by lipopolysaccharide in mice

2002 ◽  
Vol 283 (1) ◽  
pp. R218-R226 ◽  
Author(s):  
Alexander V. Gourine ◽  
Valery N. Gourine ◽  
Yohannes Tesfaigzi ◽  
Nathalie Caluwaerts ◽  
Fred Van Leuven ◽  
...  
Keyword(s):  
Mrna Level ◽  
Physiological Role ◽  
Mrna Levels ◽  
Wild Type ◽  
Cytokine Responses ◽  
Α2 Macroglobulin ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

α2-Macroglobulin (α2M) is not only a proteinase inhibitor in mammals, but it is also a specific cytokine carrier that binds pro- and anti-inflammatory cytokines implicated in fever, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). To define the role of α2M in regulation of febrile and cytokine responses, wild-type mice and mice deficient in α2M (α2M −/−) were injected with lipopolysaccharide (LPS). Changes in body temperature as well as plasma levels of IL-1β, IL-6, and TNF-α and hepatic TNF-α mRNA level during fever in α2M −/− mice were compared with those in wild-type control mice. The α2M −/− mice developed a short-term markedly attenuated (ANOVA, P < 0.05) fever in response to LPS (2.5 mg/kg ip) compared with the wild-type mice. At 1.5 h after injection of LPS, the plasma concentration of TNF-α, but not IL-1β or IL-6, was significantly lower (by 58%) in the α2M −/− mice compared with their wild-type controls (ANOVA, P < 0.05). There was no difference in hepatic TNF-α mRNA levels between α2M −/− and wild-type mice 1.5 h after injection of LPS. These data support the hypotheses that 1) α2M is important for the normal development of LPS-induced fever and 2) a putative mechanism of α2M involvement in fever is through the inhibition of TNF-α clearance. These findings indicate a novel physiological role for α2M.

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