Prostaglandin E(2) and stem cell factor can deliver opposing signals to B lymphocyte precursors.
Prostaglandin E(2) and stem cell factor can deliver opposing signals to B lymphocyte precursors.
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DOI：
10.1006/cimm.1999.1575
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发表时间：
1999-11
影响因子：
4.3
通讯作者：
T. Shimozato;P. Kincade
中科院分区：
文献类型：
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作者：
T. Shimozato;P. Kincade
合成前列腺素类16，16-二甲基PGE（2）抑制小鼠B淋巴细胞生成和正常B细胞前体或培养的F10前B细胞系向白细胞介素7的增殖。其他两种前列腺素类，PGD（2）和PGF（2 α），或PGI（2）激动剂和血栓烷A（2）激动剂受体的激动剂，则不是这种情况。PGE（2），而不是相关的前列腺素类或激动剂，诱导F10细胞凋亡。凋亡反应由EP 2类PGE（2）受体介导，需要细胞内环腺苷3 '，5'-单磷酸增加，蛋白激酶A活化和蛋白质合成。在克隆的基质细胞系或干细胞因子的存在下，PGE（2）对F10细胞的影响减弱。这些发现描述了骨髓中另一个可能影响疾病或稳态条件下B淋巴细胞生成的潜在调节回路。
The synthetic prostanoid, 16,16-dimethyl PGE(2), suppressed B lymphopoiesis in mice and proliferation of normal B cell precursors or the F10 pro-B cell line to interleukin 7 in culture. This was not the case with two other prostanoids, PGD(2) and PGF(2alpha), or agonists for PGI(2) agonist and thromboxane A(2) agonist receptors. PGE(2), but not the related prostanoids or agonists, induced apoptosis in F10 cells. The apoptotic response was mediated by the EP2 class of PGE(2) receptors and required an increase in intracellular cyclic adenosine 3',5'-monophosphate, activation of protein kinase A, and protein synthesis. The influence of PGE(2) on F10 cells was diminished in the presence of a cloned stromal cell line or stem cell factor. These findings describe another potential regulatory circuit in bone marrow which might influence B lymphopoiesis under disease or steady-state conditions.