Enhanced expression of group II phospholipase A2 gene in the tissues of endotoxin shock rats and its suppression by glucocorticoid.

Abstract

We studied the regulation of group II phospholipase A2 (PLA2-II) gene in vivo, using endotoxin shock rat as a model for systemic inflammation. Administration of endotoxin into rats increased PLA2 activity in the plasma, as described by Vadas and Hay, using endotoxin-challenged rabbit. Specific absorption of this activity by anti-PLA2-II antibody indicated that the released PLA2 was PLA2-II. The levels of PLA2-II mRNA were elevated in the aorta, spleen, lung, and thymus but not in the liver and kidney. The tissues with high PLA2-II mRNA contents released a greater amount of PLA2-II than the tissues of control rats. These results suggest that in endotoxin shock rats, PLA2-II is synthesized de novo in the above tissues and released into circulation. Furthermore, our present study demonstrates that glucocorticoid suppresses the enhanced expression of the PLA2-II gene in the tissues of endotoxin shock rats.

• Authors: T Nakano, H Arita
• Journal: FEBS letters (FEBS Lett) Vol. 273 Issue 1-2 Pg. 23-6 (Oct 29 1990) ISSN: 0014-5793 [Print] England
• PMID: 2226857 (Publication Type: Journal Article)

Chemical References

• Endotoxins
• RNA, Messenger
• Dexamethasone
• Phospholipases A
• Phospholipases A2

Topics

• Animals
• Aorta (enzymology)
• Dexamethasone (pharmacology)
• Endotoxins
• Escherichia coli
• Gene Expression (drug effects)
• Lung (enzymology)
• Male
• Muscle, Smooth, Vascular (enzymology)
• Organ Specificity
• Phospholipases A (genetics)
• Phospholipases A2
• RNA, Messenger (genetics)
• Rats
• Rats, Inbred Strains
• Reference Values
• Shock, Septic (enzymology)
• Suppression, Genetic
• Thymus Gland (enzymology)