Biotin deficiency affects the proliferation of human embryonic palatal mesenchymal cells in culture
Biotin deficiency affects the proliferation of human embryonic palatal mesenchymal cells in culture
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DOI：
10.1093/jn/138.4.680
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发表时间：
2008-04-01
影响因子：
4.2
通讯作者：
Watanabe, Toshiaki
中科院分区：
文献类型：
--
作者：
Takechi, Ryusuke;Taniguchi, Ayumi;Watanabe, Toshiaki
最近的研究表明，女性怀孕可能会导致轻微的生物素缺乏症，而没有任何临床症状。然而，人类生物素缺乏的致畸性尚未得到很好的研究。另一方面，我们以前的研究表明，母体生物素缺乏导致多种畸形，如腭裂，小颌畸形和短肢畸形，在所有的动物胎儿。然而，生物素缺乏条件下腭裂诱导的机制尚不清楚。因此，为了探讨胚胎腭裂诱导的可能机制，我们在本研究中研究了生物素缺乏对培养的人胚胎腭间充质（HEPM）细胞的影响。将HEPM细胞在生物素缺陷和生物素生理（对照）培养基中培养5周。HEPM细胞在生物素缺乏状态下的增殖可用性在培养第2周后显著降低（为对照的41.3%）。生物素缺乏的细胞中的生物素浓度显着降低后，第1周的文化，而在控制细胞保持在几乎相同的水平。生物素酶活性在生物素缺乏的细胞中也较低。全羧化酶在生物素缺乏的细胞培养的第一周后较少，几乎检测不到2周后。生物素缺乏细胞核中生物素化组蛋白的量低于对照细胞。这种抑制间充质细胞的增殖可能会延迟或抑制胚胎腭突的生长，因此它可能部分有助于腭裂诱导的机制。
It has recently been demonstrated that pregnancy in women may cause mild biotin deficiency without any clinical signs. However, the teratogenicity of biotin deficiency in humans has not been well investigated. On the other hand, our previous studies have shown that maternal biotin deficiency induces many kinds of malformations, such as cleft palate, micrognathia, and micromelia, in all animal fetuses. However the mechanism for cleft palate induction under biotin-deficient conditions is unknown. Therefore, to investigate the possible mechanisms for cleft palate induction in embryos, we investigated the effects of biotin deficiency on human embryonic palatal mesenchymal (HEPM) cells in culture in this study. HEPM cells were cultured in biotin-deficient and biotin-physiological (control) media for 5 wk. The proliferative availabilities of HEPM cells in the biotin-deficient state were significantly lower after wk 2 of culture (41.3% of the control). Biotin concentrations in biotin-deficient cells were drastically lower after wk 1 of culture, whereas those in the control cells remained at almost the same level. Biotinidase activities were also lower in biotin-deficient cells. Holocarboxylases in biotin-deficient cells were fewer after the first week of culture and were almost undetectable after wk 2. The amount of biotinylated histones in the nuclei of biotin-deficient cells was lower than in the control cells. This suppressed proliferation of mesenchymal cells may delay or inhibit the growth of palatal processes in embryos and thus it may partially contribute to the mechanisms for cleft palate induction.