GF and a SDF-production in KSP cells in cell culture. Effects of different progestogens on VEGF and SDF-1 secretion have this we found that P and various gestagens k Nnte the inhibition of E2 stimulates influence VEGF and SDF-1 production. The addition of P at a concentration of 10 9 mol / l in the culture medium had no inhibitory effect on the production of angiogenic factors by these ESC, but a h Stimulates suppressed higher concentration of P significantly E2 VEGF and SDF-1 production. As shown in Figure 4, all progestogens significantly attenuated Cht VEGF and SDF 1 production in a concentration of 109 mol / L compared with the control, w While P has these angiogenic factors in a concentration of 107 mol / l reduced, these results suggest that synthetic progestins induced inhibitory effect on E2 more VEGF and SDF-1 that P had did. Discussion The present study shows that P and progestins clinically relevant inhibitory effect on E2-induced VEGF and SDF-1 in ESCs in vitro. In addition, reverse co-treatment with the PR antagonist RU 486, the inhibition of VEGF stimulated E2 and SDF-1, which may indicate a way by which the progesterone production of these factors by reducing public relations. Earlier studies showed increased to WSR Hte release of VEGF by stimulation alone E2 and the release of VEGF and E is reduced in conjunction with MPA. Studies in ovariectomized baboons also shown that the addition of EP a stimulus induced by VEGF removed. Our study describes for the first time that different progestins attenuated Cht E-induced production of SDF. These results are consistent with previous studies describe the suppression of the SDF with a P in breast cancer cell lines and rat leiomyoma cells. As above mentioned HNT, Progestins BX-795 702675-74-9 improve the protein expression of insulin growth factor 1 binding, tissue factor, interleukin 11, interleukin 15 and fibulin 1, ESC, a well characterized model for progestin activity t. Although most studies, the P-regulated transcription is focused on the genes upregulated VEGF and SDF-1 suppression of progestins may be predicted to oppose the F Ability, the actions of E2 in the CES. In addition, k Our data, the progestational activity of t gr with a molecule can Erer accuracy than tests that exogenous journalists and / or using PR-transfected predict. Progestogens had a gr Ere effect on the production of VEGF and SDF, there P 1 at Hnlichen concentrations in the same in vitro systems. In fact, progestins generally pc Amplifiers are evaluated as P in bioassays, the maintenance of pregnancy, the inhibition of ovulation, or general effects of progestins on the endometrium rabbits. These data suggest that there is a potential difference in the human endometrium function with P and progestins may be connected. Some synthetic progestins are known to differences in receptor selective stero Dian and activity Th in its target tissues. We have not managed to show the different effects of VEGF and SDF-1 production in our experiments with different progestogens. We have shown that VEGF and SDF-stimulated E2 secretion was blocked by simultaneous treatment with Acadesine progesterone in ESCs. These results suggest that progestins reduce E2-induced angiogenic factors and suppress angiogenesis in human endometrium local. Clinical pharmacokinetics of progestogens showed that co-serum.