TUMOR-NECROSIS-FACTOR-ALPHA INHIBITS IN-VITRO DECIDUALIZATION OF HUMAN ENDOMETRIAL STROMAL CELLS
TUMOR-NECROSIS-FACTOR-ALPHA INHIBITS IN-VITRO DECIDUALIZATION OF HUMAN ENDOMETRIAL STROMAL CELLS
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DOI：
10.1093/oxfordjournals.humrep.a138460
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发表时间：
1994-12-01
影响因子：
6.1
通讯作者：
MORI, T
中科院分区：
文献类型：
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作者：
INOUE, T;KANZAKI, H;MORI, T
先前已报道白细胞介素-1 (IL-1) 可抑制人子宫内膜基质细胞的体外蜕膜化，通过孕酮诱导的催乳素产生和形态转化进行评估。在这项研究中，我们检查了其他细胞因子，如肿瘤坏死因子-α (TNF α)、干扰素-β (IFN β)、IFN γ 或粒细胞巨噬细胞集落刺激因子 (GM-CSF) 是否可以影响体外人子宫内膜基质细胞的蜕膜化。其中，TNFα以剂量依赖性方式显着抑制催乳素的产生，但对细胞数量没有明显影响。子宫内膜基质细胞的形态转化也受到TNFα的抑制。 TNFα和IL-1显着抑制子宫内膜基质细胞cAMP刺激的催乳素产生，子宫内膜基质细胞培养系统上清液中的孕酮浓度和子宫内膜基质细胞的细胞内钙浓度均不受TNFα或IL-1的添加影响。这些结果表明TNFα和IL-1抑制子宫内膜基质细胞中孕酮诱导的和cAMP介导的催乳素产生，并且这种抑制并非归因于对孕酮代谢的直接影响或与Ca2+介导的信号转导相关。这些实验表明，在体内某些病理条件下TNFα和IL-1的局部增加可能通过抑制子宫内膜基质细胞的蜕膜化来干扰囊胚植入和/或妊娠的维持。
Interleukin-1 (IL-1) has been reported previously to inhibit the in-vitro deciduaIization of human endometrial stromal cells as assessed by progesterone-induced prolactin production and morphological transformation. In this study we examined whether other cytokines, such as tumour necrosis factor-alpha (TNF alpha), interferon-beta (IFN beta), IFN gamma or granulocyte-macrophage colony-stimulating factor (GM-CSF), could affect the decidualization of human endometrial stromal cells in vitro. Of these cytokines, TNF alpha significantly suppressed prolactin production in a dose-dependent manner, with no apparent effect on cell number, The morphological transformation of endometrial stromal cells was also inhibited by TNF alpha. TNF alpha and IL-1 significantly suppressed cAMP-stimulated prolactin production by endometrial stromal cells, Neither the progesterone concentration in the supernatant of the endometrial stromal cell culture system nor intracellular calcium concentration of the endometrial stromal cells were affected by the addition of TNF alpha or IL-1. These results indicated that TNF alpha and IL-1 suppress both progesterone-induced and cAMP-mediated prolactin production in endometrial stromal cells, and that this inhibition was not attributable to direct effects on progesterone metabolism or related to Ca2+-mediated signal transduction. These experiments suggested that a local increase of TNF alpha and IL-I under certain pathological conditions in vivo may disturb blastocyst implantation and/or the maintenance of pregnancy by inhibiting the decidualization of endometrial stromal cells.