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造血微环境的研究。II. 贫血和红细胞增多症条件下小鼠骨髓和脾脏中糖胺聚糖的含量。

Studies of the haemopoietic microenvironment. II. Content of glycosaminoglycans in murine bone marrow and spleen under anaemic and polycythaemic conditions.

作者信息

Noordegraaf E M, Ploemacher R E

出版信息

Scand J Haematol. 1979 Apr 4;22(4):327-32.

PMID:472656
Abstract

Different glycosaminoglycans are described to be involved in processes of cell proliferation and differentiation. To investigate a possible direct involvement of glycosaminoglycans within the haemopoietic organs in erythropoiesis, biochemical separation and quantification of splenic and bone marrow glycosaminoglycans in anaemic and polycythaemic mice were performed. Hyaluronic acid, chondroitin sulphate A, B and C were present in both organs under both conditions. Both in spleen and bone marrow of polycythaemic mice very low amounts of chondroitin sulphate A, B and C, and a higher amount of hyaluronic acid were found in comparison to normal mice. In anaemic mice only the amount of splenic chondroitin sulphate C was found to be lower than in normal mice. It is demonstrated that considerable changes in sulphated and unsulphated glycosaminoglycans occur during erythropoietic stimulation and suppression. The present findings do not indicate a causal relationship between sulphated glycosaminoglycan levels in the haemopoietic organs and the extend of erythropoietic maturation.

摘要

不同的糖胺聚糖被认为参与细胞增殖和分化过程。为了研究糖胺聚糖在造血器官内可能直接参与红细胞生成的情况,对贫血和红细胞增多症小鼠的脾脏和骨髓糖胺聚糖进行了生化分离和定量分析。在两种情况下,透明质酸、硫酸软骨素A、B和C均存在于两个器官中。与正常小鼠相比,红细胞增多症小鼠的脾脏和骨髓中硫酸软骨素A、B和C的含量极低,而透明质酸的含量较高。在贫血小鼠中,仅发现脾脏硫酸软骨素C的含量低于正常小鼠。结果表明,在红细胞生成刺激和抑制过程中,硫酸化和非硫酸化糖胺聚糖发生了显著变化。目前的研究结果并未表明造血器官中硫酸化糖胺聚糖水平与红细胞生成成熟程度之间存在因果关系。

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Studies of the haemopoietic microenvironment. II. Content of glycosaminoglycans in murine bone marrow and spleen under anaemic and polycythaemic conditions.造血微环境的研究。II. 贫血和红细胞增多症条件下小鼠骨髓和脾脏中糖胺聚糖的含量。
Scand J Haematol. 1979 Apr 4;22(4):327-32.
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Curr Opin Hematol. 2011 Jul;18(4):239-48. doi: 10.1097/MOH.0b013e3283476140.
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Cell Tissue Res. 1988 Jun;252(3):523-31. doi: 10.1007/BF00216639.