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造血集落抑制剂由某些大鼠成纤维样细胞系产生,并受皮质类固醇调节。

Inhibitors of hematopoietic colonies are produced by certain rat fibroblastoid cell lines and are modulated by corticosteroids.

作者信息

Wang H, Sullivan A K

机构信息

McGill Cancer Centre, Montreal, Quebec, Canada.

出版信息

Exp Hematol. 1993 May;21(5):675-82.

PMID:8513870
Abstract

Both stimulatory (CSA) and inhibitory (INH) factors may contribute to hematopoietic regulation, but little is known about how their physiologic balance is maintained. Previously we have shown that antigen-defined fibroblastoid cells cultured from rat lung (ST3-/ST4+) constitutively produce INH, and those derived from bone marrow (ST3+/ST4-) respond to macrophage cytokines to release both CSA and INH into their conditioned media (CM). Here we show that this pattern was maintained in cell strains ("ST3" and "ST4") propagated from the primary cultures, and that the presence of CSA was measured in "ST4" CM if the inhibitory > 100 kd fraction was removed. Two subclones of the "ST3" line, called 2A and 9D, were selected for high or low expression of the ST3 antigen, respectively. Both produced CSA, but only 9D produced the > 100 kd inhibitor. In the CM of cells cultured in the presence of hydrocortisone, there was less INH detected but CSA was not changed. From these data, however, we cannot assess how many individual cell products might be contributing to the INH activity. These results demonstrate that the appearance of inhibitory activity in the growth media differs among fibroblast subpopulations, and that it can be modified by natural regulators such as corticosteroids.

摘要

刺激因子(CSA)和抑制因子(INH)都可能参与造血调节,但对于它们的生理平衡是如何维持的却知之甚少。此前我们已经表明,从大鼠肺培养的抗原特异性成纤维样细胞(ST3-/ST4+)可组成性产生INH,而从骨髓衍生的细胞(ST3+/ST4-)对巨噬细胞细胞因子有反应,可将CSA和INH释放到其条件培养基(CM)中。在这里我们表明,这种模式在从原代培养物传代的细胞株(“ST3”和“ST4”)中得以维持,并且如果去除抑制性的>100 kd组分,则在“ST4”CM中可检测到CSA的存在。“ST3”系的两个亚克隆,分别称为2A和9D,被选择用于分别高表达或低表达ST3抗原。两者都产生CSA,但只有9D产生>100 kd的抑制剂。在氢化可的松存在下培养的细胞的CM中,检测到的INH较少,但CSA没有变化。然而,从这些数据中,我们无法评估有多少种单独的细胞产物可能对INH活性有贡献。这些结果表明,成纤维细胞亚群在生长培养基中抑制活性的表现有所不同,并且它可以被诸如皮质类固醇等天然调节剂所改变。

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