Interleukin-1 beta and tumour necrosis factor-alpha stimulate the mRNA expression of interleukin-1 receptors in mouse anterior pituitary AtT-20 cells.
The RT-PCR technique was used to study IL-1 receptor mRNA levels in AtT-20 cells. IL-1 beta increased type I IL-1 receptor mRNA levels within 1 h, with elevated levels remaining after 24 h, whereas it induced a bell-shaped alteration of type II IL-1 receptor mRNA levels, with a peak after 6 h. Tumour necrosis factor-alpha (TNF alpha) similarly up-regulated type II IL-1 receptor mRNA levels, and type I IL-1 receptor mRNAs albeit to a lesser extent than IL-1 beta. Furthermore, IL-1 beta also induced increases in TNF alpha and c-fos mRNAs. The IL-1 receptor antagonist can fully block all the above effects of IL-1 beta. Up-regulation of type II IL-1R mRNA levels in AtT-20 cells could constitute an important way to modulate IL-1 actions, since type II IL-1R is believed to antagonize IL-1 effects.
Bristulf
J
J
Department of Neurochemistry and Neurotoxicology, Arrhenius Laboratories for Natural Sciences, Stockholm University, Sweden.
Bartfai
T
T
D000818:Animals; D015870:Gene Expression; D007375:Interleukin-1 / Q000494:pharmacology*; D051379:Mice; D010902:Pituitary Gland / Q000502:physiology*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics*; D017472:Receptors, Interleukin-1 / Q000235:genetics*; D013997:Time Factors; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D007375:Interleukin-1; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha