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首页> 外文期刊>Cellular immunology >Requirement of Smad3 for mast cell growth.
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Requirement of Smad3 for mast cell growth.

机译：Smad3对肥大细胞生长的要求。

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The involvement of the TGF-beta family in cell growth of bone marrow-derived mast cells (BMMC) cultured with medium containing pokeweed mitogen-stimulated spleen cell-conditioned medium (PWM-SCM) was examined. Doubling time of BMMC from Smad3-null mice was longer than that from wild-type (WT) mice, and the differences tended to be larger with time of culture. Consistent with the results, uptake and reduction of [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl) -2H-tetrazolium, inner sa MTS] was lower in Smad3-deficient BMMC. Cell cycle analyses revealed no apparent differences between WT BMMC and Smad3-deficient BMMC, suggesting that longer doubling time in Smad3-deficient BMMC resulted from increased cell death. TGF-beta and activin A were supplied by PWM-SCM rather than by self-production by BMMC. Blocking the TGF-beta pathway by anti-TGF-beta neutralizing antibody or an inhibitor for the type I receptors for ligands including TGF-beta and activin, SB431542, inhibited MTS uptake and reduction in WT BMMC, whereas anti-activin A antibody and SB431542 tended to inhibit them in Smad3-deficient BMMC. The present results suggest that TGF-beta-induced and Smad3-mediated signaling is essential for maximal cell growth in mast cells, and that the activin pathway may be required for it when mast cell context is modulated by Smad3 depletion.
机译：检查了TGF-β家族参与了用含有商陆有丝分裂原刺激性脾细胞条件培养基（PWM-SCM）的培养基培养的骨髓肥大细胞（BMMC）的细胞生长的过程。 Smad3无表达小鼠的BMMC加倍时间比野生型（WT）小鼠的加倍时间长，随着培养时间的延长，差异趋于更大。结果与[3-（4，5-二甲基噻唑-2-基）-5-（3-羧基甲氧基苯基）-2-（4-磺基苯基）-2H-四唑鎓内盐的摄取和还原一致; MTS]在Smad3缺陷BMMC中较低。细胞周期分析显示，WT BMMC和Smad3缺陷BMMC之间没有明显差异，这表明Smad3缺陷BMMC中更长的倍增时间是由细胞死亡增加引起的。 TGF-β和激活素A由PWM-SCM提供，而不是由BMMC自产。通过抗TGF-β中和抗体或I型受体的配体（包括TGF-β和激活素）SB431542来阻止TGF-β途径，可抑制WT BMMC的MTS摄取和减少，而抗激活素A抗体和SB431542倾向于在S​​mad3缺陷BMMC中抑制它们。目前的结果表明，TGF-β诱导和Smad3介导的信号对于肥大细胞中最大的细胞生长至关重要，并且当肥大细胞环境受Smad3耗竭调节时，可能需要激活素途径。

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