Induction of erythroid differentiation in murine erythroleukemic cells by short chain aliphatic carbonyl compounds and their corresponding precursors

Induction of erythroid differentiation in murine erythroleukemic cells by short chain aliphatic carbonyl compounds and their corresponding precursors
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短链脂肪族羰基化合物及其相应前体诱导小鼠红白血病细胞的红系分化

DOI:
10.1016/0014-5793(80)81101-x
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发表时间:
1980
期刊:
影响因子:
3.5
通讯作者:
P. Ebert
P. Ebert
中科院分区:
生物学3区
文献类型:
--
作者:
G. Malinin;P. Ebert

文献摘要

被引文献

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可通过多种化学试剂诱导原成红细胞样鼠红白血病(MEL)细胞沿红系途径分化沿着[1 -5]。红细胞分化状态通过血红蛋白合成增加和伴随的形态学变化明确识别[5,6]。虽然红细胞分化诱导信号的确切性质或细胞受体位点尚未确定[1,3],但已经提出细胞膜可能是起始位点[1,3],如某些细胞膜相关功能的变化所证明的[7,8]。我们最近已经表明SeOz和H $ eOa触发MEL细胞的红细胞分化[3],并进一步提出,内源性膜羰基化合物可能被SeO 2氧化成二羰基化合物,这可能启动了MEL细胞的红系分化。如果内源性羰基引发分化,则可能的是,所选择的外源性脂肪族羰基化合物同样可以引发MEL细胞的红系分化。此外,任何可以代谢成其相应羰基衍生物的前体也应该作为诱导物或红细胞分化。
Proerythroblastoid murine erythroleukemic (MEL) cells may be induced to differentiate along the erythroid pathway by avariety of chemical agents [l-5]. The state of erythroid differentiation is recognized unequivocally by increased hemoglobin synthesis and concomitant morphological changes [5, 6]. While the precise nature or the cellular receptor sites of the erythroid differentiation induction signal remain undetermined[1, 3], it has been suggested that the cell membrane may be the initiation site [1, 3] as evidenced by changes of certain cell membrane-related functions [7, 8].We have shown recently that SeOz and H $ eOa trigger erythroid differentiation of MEL cells [3] and suggested further, that possible oxidation by SeOz of endogenous membrane carbonyls into dicarbonyls may have initiated erythroid differentiation of MEL cells. If endogenous carbonyls are triggering differentiation, then it may be possible that selected exogenous aliphatic carbonyl compounds may likewise initiate erythroid differentiation of MEL cells. Moreover, any precursor which can be metabolized to its corresponding carbonyl derivative should also act as an inducer or erythroid differentiation.