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首页> 外文期刊>Journal of Cellular Physiology >LCN2 overexpression in bone enhances the hematopoietic compartment via modulation of the bone marrow microenvironment
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LCN2 overexpression in bone enhances the hematopoietic compartment via modulation of the bone marrow microenvironment

机译：LCN2超表达在骨增强了通过调制的造血隔间骨髓微环境

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摘要

Lipocalin-2 (LCN2) is a member of the lipocalin family whose expression is modulated in several conditions, including cell differentiation, innate immunity, stress, and cancer. Although it is known that it is expressed in bone, its function in this tissue remains poorly studied. To this end, we took advantage of transgenic mice lines that expressed LCN2 driven by a bone specific type I collagen (LCN2-Tg). In the bone marrow (BM) of LCN2-Tg mice we observed an increased number of phenotypically long-term hematopoietic stem cells (LT-HSC) that also displayed a higher proliferation rate compared to wild-type controls (Wt). Furthermore, hematopoietic progenitor cells, obtained from LCN2-Tg BM showed an increased clonogenic capacity compared to those obtained from LCN2-Tg spleen, a higher concentration of serum erythropoietin and a higher number of mature erythrocytes in the peripheral blood of old LCN2-Tg animals compared to aged-matched wt. The findings of a combined increase in the BM of the LCN2-Tg mice of SDF-1, SCF, and TIMP-1 levels along with the reduction of both MMP-9 activity and cathepsin K concentration may explain the observed effects on the HSC compartment. This study shows that LCN2 overexpression in bones modifies the BM microenvironment via modulation of the expression of key secreted factors and cytokines, which in turn regulate the HSC niche behavior enhancing both HSC homing in young mice and erythrocytes production in older mice.
机译：Lipocalin-2 lipocalin (LCN2)是一个成员调制在几个家族的表达式条件,包括细胞分化,先天免疫、压力和癌症。知道是表达在骨,它吗研究了函数在这个组织仍然不佳。为此,我们利用转基因小鼠线表示LCN2由一根骨头特定的I型胶原蛋白(LCN2-Tg)。骨髓(BM) LCN2-Tg老鼠我们观察到的一个数量的增加长期的表型造血干细胞(LT-HSC)显示更高的增殖率相比野生型控制(Wt)。造血祖细胞,获得LCN2-Tg BM显示增加单独使用从LCN2-Tg获得的能力相比脾脏,更高浓度的血清促红细胞生成素和更多的成熟外周血红细胞的老了LCN2-Tg动物相比aged-matched wt。发现的结合增加的大英博物馆SDF-1 LCN2-Tg老鼠,自洽场,TIMP-1水平随着MMP-9活动的减少和组织蛋白酶K浓度可以解释观察对HSC隔间的影响。研究表明,LCN2超表达在骨头通过调制修改大英博物馆微环境和分泌表达的关键因素细胞因子,进而调节HSC利基行为加强两HSC的年轻老鼠在年长的老鼠和红细胞生产。

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