Metallothionein induction by restraint stress: Role of glucocorticoids and IL-6

Joaquín Hernández, Javier Carrasco, Eva Belloso, Mercedes Giralt, Horst Bluethmann, Dae Kee Lee, Glen K. Andrews, Juan Hidalgo*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

52 Citations (Scopus)

Abstract

Restraint stress increased liver metallothionein-I (MT-I) mRNA and MT-I + II protein levels. The glucocorticoid receptor antagonist RU 486 decreased this response. In contrast, adrenalectomy only decreased MT-I + I protein levels. Moreover, corticosterone or progesterone did not reverse the effect of RU 486. These results suggest that glucocorticoids are important for MT-I + II protein synthesis but not for MT-I mRNA accumulation during restraint stress, and that other factors must be involved in this process. Interleukin-6 (IL-6) deficient mice showed a significant decrease of restraint stress-induced liver MT-I mRNA levels (~ 30% of IL-6+/+ mice) up to ~ 4-5 hours after the onset of stress. Western blotting of hepatic nuclear proteins showed that the IL-6 responsive transcription factor Stat3, which has been shown to mediate MT induction by inflammation, was also activated by restraint stress. Results after extended periods of restraint stress indicate that IL-6 participates early and transiently in the process. The analysis of the expression of the acute phase plasma protein serum amyloid A suggests that restraint stress elicits an acute phase response similar to that caused by inflammation. (C) 2000 Academic Press.
Original languageEnglish
Pages (from-to)791-796
JournalCytokine
Volume12
DOIs
Publication statusPublished - 1 Jan 2000

Keywords

  • Acute phase response
  • Glucocorticoids
  • Interlukin 6
  • Metallothionein
  • Stress

Fingerprint

Dive into the research topics of 'Metallothionein induction by restraint stress: Role of glucocorticoids and IL-6'. Together they form a unique fingerprint.

Cite this