scholarly journals Phyto- and Endogenous Estrogens Differently Activate Intracellular Calcium Ion Mobilization in Bovine Endometrial Cells

2006 ◽  
Vol 52 (6) ◽  
pp. 731-740 ◽  
Author(s):  
Izabela WOCLAWEK-POTOCKA ◽  
Krzysztof BORKOWSKI ◽  
Anna KORZEKWA ◽  
Kiyoshi OKUDA ◽  
Dariusz J. SKARZYNSKI
Keyword(s):  
Intracellular Calcium ◽  
Calcium Ion ◽  
Endometrial Cells ◽  
Intracellular Calcium Ion

Lysophosphatidic Acid Stimulates Prostaglandin E2 Production in Cultured Stromal Endometrial Cells Through LPA1 Receptor

2009 ◽  
Vol 234 (8) ◽  
pp. 986-993 ◽  
Author(s):  
Izabela Woclawek-Potocka ◽  
Katarzyna Kondraciuk ◽  
Dariusz Jan Skarzynski
Keyword(s):  
Epithelial Cells ◽  
Intracellular Calcium ◽  
Mrna Expression ◽  
Lysophosphatidic Acid ◽  
Stromal Cells ◽  
Calcium Ion ◽  
Cell Types ◽  
Endometrial Cells ◽  
Intracellular Calcium Ion

Lysophosphatidic acid (LPA) has been shown to be a potent modulator of prostaglandin (PG) secretion during the luteal phase of the estrous cycle in the bovine endometrium in vivo. The aims of the present study were to determine the cell types of the bovine endometrium (epithelial or stromal cells) responsible for the secretion of PGs in response to LPA, the cellular, receptor, intracellular, and enzymatic mechanisms of LPA action. Cultured bovine epithelial and stromal cells were exposed to LPA (10−5–10−9 M), tumor necrosis factor α (TNFα; 10 ng/mL) or oxytocin (OT; 10−7 M) for 24 h. LPA treatment resulted in a dose-dependent increase of PGE2 production in stromal cells, but not in epithelial cells. LPA did not influence PGF2α production in stromal or epithelial cells. To examine which type of LPA G-protein–coupled receptor (LP-GPCR; LPA1, LPA2, or LPA3) is responsible for LPA action, stromal cells were preincubated with three selected blockers of LPA receptors: NAEPA, DGPP, and Ki16425 for 0.5 h, and then stimulated with LPA. Only Ki16425 inhibited the stimulatory effect of LPA on PGE2 production and cell proliferation in the stromal cells. LPA-induced intracellular calcium ion mobilization was also inhibited only by Ki16425. Finally, we examined whether LPA-induced PGE2 synthesis in stromal cells is via the influence on mRNA expression for the enzymes responsible for PGE2 synthesis— PGE 2 synthase ( PGES) and PG-endoperoxide synthase 2 ( PTGS2). We demonstrated that the stimulatory effect of LPA on PGE2 production in stromal cells is via the stimulation of PTGS2 and PGES mRNA expression in the cells. The overall results indicate that LPA stimulates PGE2 production, cell viability, and intracellular calcium ion mobilization in cultured stromal endometrial cells via Ki16425-sensitive LPA1 receptors. Moreover, LPA exerts a stimulatory effect on PGE2 production in stromal cells via the induction of PTGS2 and PGES mRNA expression.

scholarly journals Effect of Spermidine on Intracellular Calcium Ion Mobilization in Chicken Phagocytes Treated with Leukotriene B4 (LTB4)

2005 ◽  
Vol 42 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Sheng Yong ◽  
Satoshi Isizuka ◽  
Song Han ◽  
Asaki Abe ◽  
Yasuhiro Kondo
Keyword(s):  
Intracellular Calcium ◽  
Calcium Ion ◽  
Leukotriene B4 ◽  
Intracellular Calcium Ion

scholarly journals Behavioral palatability of dietary fatty acids correlates with the intracellular calcium ion levels induced by the fatty acids in GPR120-expressing cells

2014 ◽  
Vol 35 (6) ◽  
pp. 357-367 ◽  
Author(s):  
Shin-ichi ADACHI ◽  
Ai EGUCHI ◽  
Kazuhiro SAKAMOTO ◽  
Hiroki ASANO ◽  
Yasuko MANABE ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Intracellular Calcium ◽  
Calcium Ion ◽  
Dietary Fatty Acids ◽  
Intracellular Calcium Ion

scholarly journals Platelet activating factor raises intracellular calcium ion concentration in macrophages.

1986 ◽  
Vol 103 (2) ◽  
pp. 439-450 ◽  
Author(s):  
G W Conrad ◽  
T J Rink
Keyword(s):  
Heavy Metals ◽  
Intracellular Calcium ◽  
Calcium Ion ◽  
Platelet Activating Factor ◽  
Ion Concentration ◽  
Early Event ◽  
Acetoxymethyl Ester ◽  
Intracellular Calcium Ion ◽  
The Times ◽  
Calcium Ion Concentration

Peritoneal cells from thioglycollate-stimulated mice were allowed to adhere to coverglasses for 2 h to give a dense monolayer of adherent cells greater than 95% of which were macrophages. After incubation with the tetra-acetoxymethyl ester of quin2, coverglasses were rinsed with Ca2+-free saline, oriented at a 45 degree angle in square cuvettes containing a magnetically driven stir bar, and analyzed for changes in quin2 fluorescence in a spectrofluorimeter. Such fluorescence, taken as an indication of intracellular calcium ion concentration ([Ca2+]i), increased as exogenous calcium ion concentration ([Ca2+]o) was raised to 1 mM. At [Ca2+]o approximately equal to 10 microM, [Ca2+]i = 72 +/- 14 nM (n = 26); at [Ca2+]o = 1 mM, [Ca2+]i = 140-220 nM, levels not increased by N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine, a membrane-permeant chelator of heavy metals than can quench quin2. Addition of mouse alpha + beta fibroblast interferon, lipopolysaccharide, thrombin, collagen, vasopressin, ADP, compound 48/80, or U46619 did not change [Ca2+]i. However, addition of platelet activating factor (PAF) (2-20 ng/ml) raised [Ca2+]i by 480 nM within 1 min if [Ca2+]o = 1 mM. In the presence of 5 mM EGTA, PAF raised [Ca2+]i by 25 nM. This suggests that PAF causes influx of exogenous Ca2+, as well as releasing some Ca2+ from intracellular stores. Consistent with these results, when PAF was added to 1 mM Ca2+ in the presence of 100 microM Cd2+ or Mn2+ to block Ca2+ influx, [Ca2+]i increased by only intermediate amounts; at the times of such dampened peak response, [Ca2+]i could be raised within 1 min to normal PAF-stimulated levels by chelation of the exogenous heavy metals with diethylenetriaminepentaacetic acid. Normal PAF responses were observed in the presence of indomethacin. The lowest dose of PAF observed to raise [Ca2+]i was 0.1 ng/ml. Response of [Ca2+]i to 2-20 ng/ml PAF was transient, and second applications had no effect. The PAF response also was seen in cell suspensions. These results suggest that an increase in [Ca2+]i may be an early event in PAF activation of macrophages.

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