COMPARATIVE-STUDIES OF THE GRANULOPOIETIC ENHANCING EFFECTS OF BIOSYNTHETIC HUMAN INSULIN-LIKE GROWTH FACTOR-I AND FACTOR-II
COMPARATIVE-STUDIES OF THE GRANULOPOIETIC ENHANCING EFFECTS OF BIOSYNTHETIC HUMAN INSULIN-LIKE GROWTH FACTOR-I AND FACTOR-II
复制标题
DOI：
10.1002/jcp.1041570123
复制
发表时间：
1993-10-01
影响因子：
5.6
通讯作者：
SKOTTNER, A
中科院分区：
文献类型：
--
作者：
MERCHAV, S;LAKE, M;SKOTTNER, A
研究了生物合成的人胰岛素样生长因子I（IGF-I）和IGF-II在重组人粒细胞集落刺激因子（rhG-CSF）、粒细胞-巨噬细胞集落刺激因子（rhGM-CSF）和白细胞介素-3（rhIL-3）存在下对人骨髓祖细胞体外生长的影响。IGF-I和IGF-II类似地增强了用任何上述造血调节剂刺激的培养物中的骨髓祖细胞的生长。集落组成分析显示粒细胞集落数量增加，但巨噬细胞或粒细胞/巨噬细胞集落数量无变化。在G-CSF、GM-CSF或IL-3存在下，IGF-I分别诱导粒细胞集落数增加62 +/-16%、84 +/-13%和107 +/- 18%。IGF-II的值分别为66 +/-13%、96 +/-12%和91 +/-12%。在已经去除辅助细胞的骨髓细胞的G-CSF和GM-CSF刺激的培养物中也检测到两种肽对骨髓集落形成的类似增强，而在IL-3存在下，两种肽在这种培养物中均不发挥任何作用。IGF-I和IGF-II的促生长作用被针对IGF-I（I型）膜受体的单克隆抗体完全消除。因此，IGF-I和IGF-II似乎通过涉及I型受体的直接机制对人骨髓髓样祖细胞发挥作用。(C)1993 Wiley-Liss，Inc.
The effect of biosynthetic human insulin-like growth factor I (IGF-I) and IGF-II on the in vitro growth of human marrow myeloid progenitors in the presence of recombinant human granulocyte colony stimulating factor (rhG-CSF), granulocyte-macrophage CSF (rhGM-CSF), or interleukin-3 (rhIL-3), was investigated. IGF-I and IGF-II similarly enhanced the growth of myeloid progenitors in cultures stimulated with any of the above hemopoietic regulators. Analysis of colony composition showed an increase in the numbers of granulocyte colonies, but no alteration in the numbers of macrophage or granulocyte/macrophage colonies. IGF-I induced an increase of 62 +/- 16%, 84 +/- 13%, and 107 +/- 18% in granulocyte colony numbers in the presence of G-CSF, GM-CSF, or IL-3, respectively. The values for IGF-II were 66 +/- 13%, 96 +/- 12%, and 91 +/- 12%. Similar enhancement of myeloid colony formation by both peptides was also detected in G-CSF and GM-CSF-stimulated cultures of marrow cells that had been depleted of accessory cells, while neither peptide exerted any effect in the presence of IL-3 in such cultures. The growth-promoting effects of IGF-I and IGF-II were completely abrogated by monoclonal antibodies directed against the IGF-I (Type I) membrane receptor. IGF-I and IGF-II thus appear to exert their effects on human marrow myeloid progenitors via a direct mechanism involving the Type I receptor. (C) 1993 Wiley-Liss, Inc.