Comparison of the effects of tumour necrosis factor α stimulation and phorbol ester treatment on the immunocytochemical staining of intercellular adhesion molecule 1 in human renal carcinoma cell cultures

1993 ◽  
Vol 63 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Alastair B. Hansen ◽  
Claus B. Andersen
Keyword(s):  
Tumour Necrosis ◽  
Renal Carcinoma ◽  
Carcinoma Cell ◽  
Intercellular Adhesion Molecule ◽  
Immunocytochemical Staining ◽  
Tumour Necrosis Factor Α ◽  
Intercellular Adhesion Molecule 1 ◽  
Factor Α ◽  
Necrosis Factor ◽  
Human Renal Carcinoma

scholarly journals The effects of tumour necrosis factor-α and interleukin1 on an in vitro model of thyroid-associated ophthalmopathy; contrasting effects on adipogenesis

2006 ◽  
Vol 155 (3) ◽  
pp. 395-403 ◽  
Author(s):  
T J Cawood ◽  
P Moriarty ◽  
C O’Farrelly ◽  
D O’Shea
Keyword(s):  
Hyaluronic Acid ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Intercellular Adhesion Molecule ◽  
Tumour Necrosis Factor Α ◽  
Intercellular Adhesion Molecule 1 ◽  
Thyroid Associated Ophthalmopathy ◽  
Factor Α ◽  
Necrosis Factor

Objective: Cytokines are likely to play a key pathogenic role in thyroid-associated ophthalmopathy (TAO). Anti-cytokine therapy has been proposed to be a possible treatment for active TAO. We aimed to establish the effects of selected cytokines on intercellular adhesion molecule 1 (ICAM1) expression, glycosaminoglycan (GAG) production and adipogenesis in orbital fibroblasts (OFs) from patients with TAO. Methods: Orbital tissue was taken during surgery from eight patients with TAO and five control subjects. OFs were cultured and ICAM1 expression measured by flow cytometry. GAG production was measured by hyaluronic acid ELISA. OFs were grown in adipogenic media and the degree of adipogenesis quantified. Results: Responses were similar in OFs from patients with and without TAO. Tumour necrosis factor-α (TNFα) and interleukin1 (IL1) (0.1 ng/ml) stimulated ICAM1 expression by eight- to ten-fold. Anti-cytokine agents inhibited the cytokine-upregulated ICAM1 expression by 90–99% (P<0.01). TNFα and IL1 (0.1 ng/ml) increased hyaluronic acid production by 44 and 95% (P<0.01) respectively. Anti-cytokine agents inhibited these responses by 79–138% (P<0.04). TNFα (0.1 ng/ml) inhibited adipogenesis (−0.013 AU and −1.0; P<0.03) whilst IL1 (0.1 ng/ml) stimulated adipogenesis (+0.05 AU and +5.7; P<0.02) measured by oil-red-O extraction and visual assessment respectively. The anti-IL1 agent inhibited IL1-mediated adipogenesis by 69–106% (P<0.04). Conclusion: TNFα and IL1 stimulate ICAM1 expression and GAG production, but have opposite effects on adipogenesis in OFs in vitro. IL1 promotes adipogenesis and its effects can be blocked by anti-IL1 agents in vitro. These agents may be the anti-cytokine treatment of choice for clinical trials in active TAO.

scholarly journals Ambient but not incremental oxidant generation effects intercellular adhesion molecule 1 induction by tumour necrosis factor α in endothelium

1998 ◽  
Vol 331 (3) ◽  
pp. 853-861 ◽  
Author(s):  
Toshiyuki ARAI ◽  
Susan A. KELLY ◽  
Matthew L. BRENGMAN ◽  
Manabu TAKANO ◽  
Elise H. SMITH ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Adhesion Molecule ◽  
Tumour Necrosis ◽  
Intercellular Adhesion Molecule ◽  
Tumour Necrosis Factor Α ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Proinflammatory cytokines upregulate endothelial adhesion molecule expression, thereby initiating the microvascular inflammatory response. We re-evaluated the reported role of reactive oxygen metabolites (ROMs) in signalling upregulation of intercellular adhesion molecule 1 (ICAM-1) on endothelial cells by tumour necrosis factor α (TNF-α) in vitro. TNF-α upregulation of endothelial-cell ICAM-1 expression was inhibited by the cell-permeable antioxidants, or by the adenovirus-mediated intracellular overexpression of Cu,Zn-superoxide dismutase, but not by the exogenous (extracellular) administration of the cell-impermeable antioxidants, superoxide dismutase and/or catalase. This ICAM-1 upregulation was also inhibited by inhibitors of NADH dehydrogenase, cytochrome bc1 complex and NADPH oxidase. However, a measurable increase in net cellular ROM generation in response to TNF-α was not seen using four disparate sensitive ROM assays. Moreover, the stimulation of exogenous or endogenous ROM generation did not upregulate ICAM-1, nor enhance ICAM-1 upregulation by TNF-α. These findings suggest that an ambient background flux of ROMs, generated intracellularly, but not their net incremental generation, is necessary for TNF-α to induce ICAM-1 expression in endothelium in vitro.

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