EFFECT OF LEUKEMIA INHIBITORY FACTOR ON HUMAN CYTOTROPHOBLAST DIFFERENTIATION ALONG THE INVASIVE PATHWAY
EFFECT OF LEUKEMIA INHIBITORY FACTOR ON HUMAN CYTOTROPHOBLAST DIFFERENTIATION ALONG THE INVASIVE PATHWAY
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DOI：
10.1111/j.1600-0897.1995.tb00945.x
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发表时间：
1995-10-01
影响因子：
3.6
通讯作者：
CAMPANA, A
中科院分区：
文献类型：
--
作者：
BISCHOF, P;HAENGGELI, L;CAMPANA, A
问题：白血病抑制因子 (LIF) 是一种多效性分泌细胞因子，已被证明对于小鼠囊胚植入至关重要。由于有充分证据表明 LIF 是由人子宫内膜产生的，我们想知道这种细胞因子是否能够调节人细胞滋养细胞 (CTB) 的侵袭行为。方法：从妊娠早期流产中分离和纯化 CTB，使用特定的单克隆抗体和磁性颗粒将其分离或不分离到带有层粘连蛋白或纤连蛋白受体（分别为 α 6 β 4 或 α 5 β 1 ）的细胞中。结果：我们观察到rhLIF 抑制 CTB 的明胶酶和 hCG 分泌，但对胎儿纤连蛋白 (fFN) 的分泌没有影响。这些作用作用于不同的CTB亚群：虽然rhLIF抑制α6阳性细胞分泌明胶酶，但它刺激α5阳性细胞分泌fFN。 rhLIF对hCG分泌的抑制作用主要是由于其对α5阳性CTB的hCG分泌的影响。结论：综合这些结果表明，体外LIF通过抑制金属蛋白酶的分泌、增加fFN向细胞外基质的沉积以及抑制CTB向合胞体的分化来抑制CTB向侵袭表型的分化。
PROBLEM: Leukemia inhibitory factor (LIF) is a pleiotropic secreted cytokine that was shown to be essential for blastocyst implantation in mice. Since it is well documented that LIF is produced by the human endometrium, we wondered if this cytokine was capable of modulating the invasive behaviour of human cytotrophoblastic cells (CTB).METHODS: CTB were isolated and purified from first trimester abortions, separated or not into cells bearing a laminin or a fibronectin receptor (alpha 6 beta 4 or alpha 5 beta 1 respectively) using specific monoclonal antibodies and magnetic particles.RESULTS: We observed that rhLIF inhibited the secretion of gelatinases and of hCG by CTB but remained without effects on the secretion of fetal fibronectin (fFN). These effects were exerted on different CTB subsets: although rhLIF inhibited the secretion of gelatinases by alpha 6 positive cells, it stimulated the fFN secretion by alpha 5 positive cells. The inhibitory effect of rhLIF on the secretion of hCG was mainly due to its effect on the hCG secretion of alpha 5 positive CTB.CONCLUSIONS: Taken together these results suggest that in vitro LIF inhibits the differ entiation of CTB towards an invasive phenotype by inhibiting the secretion of metalloproteinases, by increasing the deposition of fFN into the extracellular matrix and by inhibiting the differentiation of CTB into syncytium.