scholarly journals Effects of Bradykinin on the Regulatory Mechanism of PGI2 Synthesis in Human Vascular Endothelial Cells with Reference to the Intracellular Ca2+ Kinetics and mRNA Expression of Cytosolic Phospholipase A2 (cPLA2) and Prostaglandin H2 Synthase-1 (PGHS-1)

1998 ◽  
Vol 9 (1) ◽  
pp. 52-63
Author(s):  
Seiki YAMASAKI ◽  
Shohei SAWADA ◽  
Yoshihito KONO ◽  
Tadashi HIGAKI ◽  
Yusuke TADA ◽  
...  
Endocrinology ◽  
2006 ◽  
Vol 147 (5) ◽  
pp. 2490-2495 ◽  
Author(s):  
Wenjiao Li ◽  
Lu Gao ◽  
Yan Wang ◽  
Tao Duan ◽  
Leslie Myatt ◽  
...  

Chorion is the most abundant site of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression within intrauterine tissues. It is important to study the regulation of 11β-HSD1 expression in the chorion in terms of local cortisol production during pregnancy. Using real-time PCR and enzyme activity assay, we found that cortisol (1 μm) and IL-1β (10 ng/ml) for 24 h significantly increased 11β-HSD1 mRNA expression and reductase activity in cultured human chorionic trophoblasts. A further significant increase of 11β-HSD1 mRNA expression and reductase activity was observed with cotreatment of cortisol and IL-1β. To explore the mechanism of induction, 11β-HSD1 promoter was cloned into pGL3 plasmid expressing a luciferase reporter gene. By transfecting the constructed vector into WISH cells, an amnion-derived cell line, we found that cortisol (1 μm) or IL-1β (10 ng/ml) significantly increased reporter gene expression. Likewise, an additional increase in reporter gene expression was observed with cotreatment of cortisol and IL-β. To explore the physiological significance of 11β-HSD1 induction in the chorion, we studied the effect of cortisol on cytosolic phospholipase A2 and cyclooxygenase 2 expression. We found that treatment of chorionic trophoblast cells with cortisol (1 μm) induced both cytosolic phospholipase A2 and cyclooxygenase 2 mRNA expression. We conclude that cortisol up-regulates 11β-HSD1 expression through induction of promoter activity, and the effect was enhanced by IL-1β, suggesting that more biologically active glucocorticoids could be generated in the fetal membranes in the presence of infection, which may consequently feed forward in up-regulation of prostaglandin synthesis.


1996 ◽  
Vol 218 (2) ◽  
pp. 500-504 ◽  
Author(s):  
Michael J. Pearce ◽  
Thomas M. McIntyre ◽  
Stephen M. Prescott ◽  
Guy A. Zimmerman ◽  
Ralph E. Whatley

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