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The murine growth differentiation factor 15 is not essential for systemic iron homeostasis in phlebotomized mice

机译:小鼠生长分化因子15对于采血小鼠的全身铁稳态不是必需的

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摘要

In conditions of increased erythropoiesis, expression of hepcidin, the master regulator of systemic iron homeostasis, is decreased to allow for the release of iron into the blood stream from duodenal enterocytes and macrophages. It has been suggested that hepcidin suppression is controlled by growth differentiation factor 15 (GDF15), a member of the transforming growth factor-β superfamily of cytokines that is secreted from developing erythroblasts. In this study, we analyzed iron-related parameters in mice deficient for GDF15 under steady-state conditions and in response to increased erythropoietic activity induced by blood loss. We demonstrate that GDF15 suppresses the hepatic mRNA expression of some BMP/TGFβ target genes but not of hepcidin, and show that GDF15 is not required to balance iron homeostasis in response to blood loss.
机译:在促红细胞生成增加的情况下,铁调素(系统铁稳态的主要调节剂)的表达降低,以允许铁从十二指肠肠上皮细胞和巨噬细胞释放到血流中。已经提出,铁调素的抑制是由生长分化因子15(GDF15)控制的,GDF15是发育中的成红细胞分泌的细胞因子的转化生长因子-β超家族的成员。在这项研究中,我们分析了在稳态条件下以及对失血引起的促红细胞生成活动增加的反应中,缺乏GDF15的小鼠的铁相关参数。我们证明GDF15抑制某些BMP /TGFβ靶基因的肝mRNA表达,但不抑制铁调素,并表明GDF15不需要平衡铁稳态以应对失血。

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