The study of cytokines, as a regulator on the proliferation, invasion and differentiation of trophoblasts.

用携带SV40大T基因的ZipNeoSV(X)重组逆转录病毒载体ZipSV4O-6和标志基因新霉素乙酰转移酶分别感染原代滋养层细胞和蜕膜来源细胞。(1)肿瘤坏死因子-α呈剂量依赖性抑制DNA合成，对孕酮合成无影响。(2)IL-β对DNA合成和孕酮合成均无影响。(3)TCL条件培养液可抑制DE-1合成PGE2，但不影响DE-1的DNA含量。(5)单核细胞白血病细胞系THP-1减弱了DE-1对TCL孕酮合成和DNA含量的影响。结果表明，肿瘤坏死因子-α对蜕膜和滋养层细胞的功能和增殖均有调节作用，滋养层细胞抑制蜕膜细胞合成PGE_2而不影响蜕膜细胞的增殖，蜕膜细胞抑制滋养层细胞的增殖，而促进滋养层细胞孕酮的合成。此外，THP-1对滋养层细胞和蜕膜细胞之间的相互作用也有影响。

The vector ZipSV4O-6, a recombinant retrovirus derived from ZipNeoSV(X) carrying the SV40 large T gene and the marker gene neomycin acetyl transferase were used to infect primary trophoblast and decidua derived cells, respectivelly. (1)TNF-alpha dose-dependently decreased DNAsynthesis without any effect on progesterone synthe-sis. (2)IL-beta has no effect on both DNA and progesterone synthesis. (3)TCL conditioned medium decreased PGE2 synthesis by DE-1 without affecting DNA content in DE-1. (4)DE-1 conditioned medium increased progesterone synthesis by TCL, whereas that decreased DNA content in TCL.(5)THP-1, which is the cell line derived from monocytic leukemia, attenuated the action of DE-1 on progesterone synthesis and DNA content in TCL.These results indicate that TNF-a regulates the function and proliferation both of decidual and trophoblast cells, that trophoblasts inhibit PGE2 synthesis by decidual cells withou affecting proliferation of decidual cells, and that decidual cells inhibit proliferation of trophoblasts whereas that stimulate progesterone synthesis by trophoblasts. Moreover, it was indicated that THP-1 had effects on the mutual actions between trophoblasts and decidual cells.