miRNA let-7 expression is regulated by glucose and TNF-α by a remote upstream promoter

2015 ◽  
Vol 472 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Mutsumi Katayama ◽  
Rasmus J.O. Sjögren ◽  
Brendan Egan ◽  
Anna Krook
Keyword(s):  
Tumour Necrosis Factor ◽  
Promoter Region ◽  
Tumour Necrosis ◽  
Promoter Activity ◽  
Family Members ◽  
Putative Promoter ◽  
Putative Promoter Region ◽  
Upstream Promoter ◽  
Tnf Α ◽  
Necrosis Factor

We investigated the putative promoter region of miRNA let-7a-1/f-1/d cluster, determined promoter activity and identified a novel promoter area for these three let-7 family members expressed. We provide evidence that let-7 expression is regulated by insulin and tumour necrosis factor (TNF)-α.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

scholarly journals Pregnancy in Takayasu Arteritis Patients Exposed to Anti-Tumour Necrosis Factor (Anti-TNF)-α Therapy

2016 ◽  
Vol 2 (5) ◽  
pp. 96-98
Author(s):  
Valentina Canti ◽  
◽  
Elena Baldissera ◽  
Susanna Rosa ◽  
Giuseppe A. Ramirez ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Takayasu Arteritis ◽  
Tumour Necrosis ◽  
Tnf Α ◽  
Necrosis Factor

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

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