The effects of differentiation and glucocorticoid treatment on the expression of lipocortin 1 in U937 cells.
- Author:
Young Joo CHO
;
Hee Bom MOON
;
Do Sun NA
- Publication Type:In Vitro ; Original Article
- MeSH:
Annexin A1*;
Annexins*;
Arachidonic Acid;
Cell Lineage;
Cell Proliferation;
Dexamethasone;
Humans;
Hydrocortisone;
Macrophages;
Neutrophils;
Phospholipases A2;
Platelet Activating Factor;
RNA, Messenger;
Signal Transduction;
U937 Cells*
- From:Korean Journal of Allergy
1997;17(2):119-128
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Lipocortin represents a family of similar Ca++ depentent phospholipid-binding proteins capable of blocking the activity of phospholipase A2 (PLA2) in vitro. Generally, these proteins are believed to inhibit the release of arachidonic acid from photopholipids and the formation of lipid mediators such as prostaglandin, leukotriene, and platelet activating factor. Lipocortin 1, initially identified as a glucocorticoid- responsive protein in macrophages and neutrophils has been implicated in transmembrane signal transduction during growth factor-mediated cell proliferation and transformation. To define the synthesis and its regulation, we investigated the expression of lipocortin 1 in both the mRNA and protein level in U937 cell line in the presence of several differentiation factors. The results were as follows. 1. The expression of lipocortin 1 and its mRNA was increased during TPA-induced differentiation of U937 cells to maximum of 2-fold and 5-fold respectively. Both the protein and mRNA levels decreased after 48 hours. 2. With the treatment with IFN-gamma, the expression of CD16 was increased. However, the protein and mRNA levels of lipocortin 1 were, not changed significantly. 3. Neither the dexamethasone or hydrocortisone have any effects on the expression of lipocortin 1 in both TPA-differentiated and undifferentiated U937 cells. The results from this study would give a light on defining the functional role of lipocortin 1 in macro-moncycle cell lineage and possibly some informative clues for the pathogenic mechanisms of the inflammatory diseases.
