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一种新的基于成熟度的中性粒细胞祖细胞分群方法,适用于骨髓增生异常综合征的研究。

A new method for maturity-dependent fractionation of neutrophil progenitors applicable for the study of myelodysplastic syndromes.

机构信息

Department of Pharmacology, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima 960-1295, Japan.

出版信息

Biomark Res. 2014 Jan 22;2(1):2. doi: 10.1186/2050-7771-2-2.

DOI:10.1186/2050-7771-2-2
PMID:24451620
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3904161/
Abstract

We applied our new method, maturity-dependent fractionation of bone marrow-derived neutrophil progenitors, to a study of gene expression profiles during granulopoiesis in myelodysplastic syndromes. CD34+ cells with low density [F1], CD11b-/CD16- [F2], CD11b+/CD16- [F3] and CD11b+/CD16low [F4] with intermediate density, CD11b+/CD16int [F5] and CD11b+/CD16high [F6] with high density were isolated from six patients. Although AML1 and C/EBP-ϵ mRNA peaked at F1 and F4, respectively, in healthy individuals, C/EBP-ϵ was maximized at F2/F3 in all patients, two of whom showed simultaneous peaks of AML1 at F2. Thus, this fractionation is useful to detect mistimed induction of granulopoiesis-regulating genes in myelodysplastic syndromes.

摘要

我们应用新的方法,即骨髓源性中性粒细胞前体的成熟依赖性分离,研究骨髓增生异常综合征中粒细胞生成过程中的基因表达谱。从六位患者中分离出低密度的 CD34+细胞 [F1]、CD11b-/CD16- [F2]、CD11b+/CD16- [F3] 和 CD11b+/CD16low [F4]、中密度的 CD11b+/CD16int [F5] 和 CD11b+/CD16high [F6]。尽管 AML1 和 C/EBP-ϵ mRNA 在健康个体中分别在 F1 和 F4 达到峰值,但在所有患者中 C/EBP-ϵ 在 F2/F3 达到最大值,其中两位患者在 F2 时同时出现 AML1 的峰值。因此,这种分离方法可用于检测骨髓增生异常综合征中粒细胞生成调节基因的时机不当诱导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbb6/3904161/08d094d45631/2050-7771-2-2-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbb6/3904161/08d094d45631/2050-7771-2-2-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dbb6/3904161/08d094d45631/2050-7771-2-2-1.jpg

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本文引用的文献

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Exp Hematol. 2012 Aug;40(8):675-81. doi: 10.1016/j.exphem.2012.03.003. Epub 2012 Apr 5.
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Myelodysplastic syndromes.骨髓增生异常综合征。
Annu Rev Med. 2010;61:345-58. doi: 10.1146/annurev.med.051308.132852.
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Relationship of differential gene expression profiles in CD34+ myelodysplastic syndrome marrow cells to disease subtype and progression.
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