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首页> 外文期刊>Translational research: the journal of laboratory and clinical medicine >Placental growth factor attenuates suppression of erythroid colony formation by interferon.
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Placental growth factor attenuates suppression of erythroid colony formation by interferon.

机译：胎盘生长因子减弱了干扰素对红系集落形成的抑制作用。

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Placental growth factor (PlGF) is a member of the vascular endothelial growth factor family and is associated with inflammation and with pathologic angiogenesis. PlGF is released from marrow erythroid cells, and serum PlGF concentrations have been reported to distinguish sickle cell patients from healthy controls. We observed that erythroid colony forming units (CFU-Es) from homozygous sickle cell (SS) patients are less sensitive to inhibition by rhgammaIFN than those from healthy controls, and the contribution of PlGF to this process was evaluated. At 10-1000-pg/mL concentrations, PlGF neither inhibits nor enhances CFU-E colony formation, and no differences were observed between the responses of SS patients or healthy controls. rhPlGF 100 pg/mL reversed the inhibitory effects of rhgammaIFN on CFU-E colony formation. rhPlGF significantly attenuated rhgammaIFN induction of the Fas ligand in an erythroid cell line (HCD57). Both HCD57 cells and CD36+ human marrow cells express Flt-1, which is a receptor for PlGF. A neutralizing antibody against Flt-1 partially attenuated the IFN-protective effect of rhPlGF, although this effect was not statistically significant. In conclusion, increased PlGF concentrations in the marrow of SS patients may protect erythroid progenitors from cytokine-induced inhibition of colony formation, and it may be a mechanism by which erythropoiesis in sickle cell disease is preserved despite concurrent inflammation.
机译：胎盘生长因子（PlGF）是血管内皮生长因子家族的成员，与炎症和病理性血管生成有关。 PlGF从骨髓红系细胞释放，并且据报道血清PlGF浓度可将镰状细胞患者与健康对照区分开。我们观察到纯合的镰状细胞（SS）患者的类红细胞集落形成单位（CFU-Es）对rhgammaIFN的抑制作用比健康对照者更不敏感，并且评估了PlGF对这一过程的贡献。在10-1000-pg / mL的浓度下，PlGF既不抑制也不增强CFU-E集落的形成，并且在SS患者或健康对照组的反应之间未观察到差异。 rhPlGF 100 pg / mL逆转了rhgammaIFN对CFU-E集落形成的抑制作用。 rhPlGF显着减弱了红系细胞系（HCD57）中Fas配体的rhgammaIFN诱导。 HCD57细胞和CD36 +人类骨髓细胞均表达Flt-1，它是PlGF的受体。尽管针对Flt-1的中和性抗体在统计学上不显着，但它会部分减弱rhPlGF对IFN的保护作用。总之，SS患者骨髓中PlGF浓度的增加可以保护类红细胞祖细胞免受细胞因子诱导的集落形成的抑制，这可能是镰状细胞疾病中尽管存在并发炎症仍能保持红细胞生成的机制。

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