Oxoanions stimulate in vitro ovulation and signal transduction pathways in goldfish (Carassius auratus) follicles

1992 ◽  
Vol 263 (5) ◽  
pp. E943-E949 ◽  
Author(s):  
S. Y. Hsu ◽  
F. W. Goetz

The present study investigated the effects of a number of oxoanion compounds on in vitro ovulation of goldfish follicles and ovarian second messenger activities. Significant levels of ovulation were induced by 0.1 mM sodium chromate, 0.1 mM sodium metavanadate, 10 mM sodium molybdate, 0.1 mM sodium orthovanadate, 5 mM sodium selenate, 0.5 mM sodium tungstate, and 0.1 mM vanadyl sulfate. At levels that significantly stimulated ovulation, metavanadate, molybdate, orthovanadate, tungstate, and vanadyl sulfate also stimulated follicular phosphatidylinositol cycling and inhibited ovarian alkaline phosphatase activity. Moreover, the ovulation induced by these oxoanions was not inhibited by indomethacin (10 micrograms/ml), while ovulation induced by selenate and chromate was. In contrast, only vanadium-containing compounds significantly stimulated prostaglandin (PG) synthesis, and, in fact, selenate significantly inhibited PG production. Finally, only sodium molybdate- and vanadium-containing compounds appeared to increase follicular adenosine 3',5'-cyclic monophosphate content. While all oxoanions stimulated in vitro ovulation, they had differential effects on certain signal transduction pathways when tested at concentrations that stimulated in vitro ovulation. From the results, two basic groups could be delineated, one containing tungstate-, molybdate-, and vanadium-containing compounds and the other selenate and chromate. Thus the mechanism by which ovulation is induced by chromate and selenate may be different from that of vanadium-containing compounds, molybdate, and tungstate.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood ◽  
2000 ◽  
Vol 96 (3) ◽  
pp. 1039-1046 ◽  
Author(s):  
Kirit M. Ardeshna ◽  
Arnold R. Pizzey ◽  
Stephen Devereux ◽  
Asim Khwaja

Abstract As a dendritic cell (DC) matures, it becomes more potent as an antigen-presenting cell. This functional change is accompanied by a change in DC immunophenotype. The signal transduction events underlying this process are poorly characterized. In this study, we have investigated the signal transduction pathways involved in the lipopolysaccharide (LPS)-induced maturation of human monocyte–derived DCs (MoDCs) in vitro. We show that exposure of immature MoDCs to LPS activates the p38 stress-activated protein kinase (p38SAPK), extracellular signal–regulated protein kinase (ERK), phosphoinositide 3-OH kinase (PI3 kinase)/Akt, and nuclear factor (NF)-κB pathways. Studies using inhibitors demonstrate that PI3 kinase/Akt but not the other pathways are important in maintaining survival of LPS-stimulated MoDCs. Inhibiting p38SAPK prevented activation of the transcription factors ATF-2 and CREB and significantly reduced the LPS-induced up-regulation of CD80, CD83, and CD86, but did not have any significant effect on the LPS-induced changes in macropinocytosis or HLA-DR, CD40, and CD1a expression. Inhibiting the NF-κB pathway significantly reduced the LPS-induced up-regulation of HLA-DR as well as CD80, CD83, and CD86. Inhibiting the p38SAPK and NF-κB pathways simultaneously had variable effects depending on the cell surface marker studied. It thus appears that different aspects of LPS-induced MoDC maturation are regulated by different and sometimes overlapping pathways.


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