Inhibition of cAMP inhibits PGE2-induced CXCR4 expression on HMECs
Stimulant . | CXCR4, MFI . |
|---|---|
| None | 121 ± 32 |
| PGE2 | 328 ± 53 |
| PGE2 + adenosine-3′,5′-cyclic monophosphorothioate, Rp-isomer | 178 ± 48* |
| PGE2 + adenosine-3′,5′-cyclic monophosphorothioate, 8-bromo-Rp-isomer | 168 ± 43* |
Stimulant . | CXCR4, MFI . |
|---|---|
| None | 121 ± 32 |
| PGE2 | 328 ± 53 |
| PGE2 + adenosine-3′,5′-cyclic monophosphorothioate, Rp-isomer | 178 ± 48* |
| PGE2 + adenosine-3′,5′-cyclic monophosphorothioate, 8-bromo-Rp-isomer | 168 ± 43* |
HMECs were stimulated with PGE2 (1 × 10-9 M). Then, adenosine-3′,5′-cyclic monophosphorothioate, Rp-isomer (50 μM) or adenosine-3′,5′-cyclic monophosphorothioate, 8-bromo-Rp-isomer (100 μM) was added and cells were incubated for 24 hours. Thereafter, the cell surface expression of CXCR4 was analyzed. The background level of fluorescence intensity (MFI) in the presence of mouse IgG2a control was subtracted. The mean + SEM of 3 experiments is shown.
P < .01 as compared with PGE2-induced CXCR4 expression.