Reactivation of a hematopoietic endocrine program of pregnancy contributes to recovery from thrombocytopenia
Reactivation of a hematopoietic endocrine program of pregnancy contributes to recovery from thrombocytopenia
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DOI：
10.1210/me.16.6.1386
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发表时间：
2002-06-01
影响因子：
--
通讯作者：
Linzer, DIH
中科院分区：
文献类型：
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作者：
Bhattacharyya, S;Lin, JD;Linzer, DIH
血小板水平的调节涉及一系列细胞因子，包括胎盘激素 PRL 样蛋白 E (PLP-E)。 PLP-E 受体存在于怀孕小鼠、非怀孕雌性小鼠和雄性小鼠的巨核细胞上。其他已知的巨核细胞细胞因子不具有 PLP-E 受体，因此非妊娠动物中该受体的存在表明 PLP-E 可能在胎盘以外的组织中表达。与这一预测一致，PLP-E 在血小板减少的小鼠骨髓中产生，主要在粒细胞中产生，但在正常小鼠骨髓中不产生。血小板减少小鼠的血清、纯化的血小板生成素或 IL-6 或妊娠可诱导骨髓细胞表达 PLP-E。血小板减少症引起的 PLP-E 基因表达的诱导具有生理意义，因为将 PLP-E 注射到血小板减少症小鼠中可以恢复正常的血小板水平，而对粒细胞、红细胞和白细胞总数没有影响。我们得出的结论是，骨髓中 PLP-E 的诱导表达是血小板减少症恢复机制的一部分。这些结果还提出了一个更普遍的概念：怀孕的内分泌程序在哺乳动物中已经进化以支持胎儿的宫内生长和发育，也可以用来响应病理生理学。
Regulation of blood platelet levels involves an array of cytokines, including the placental hormone PRL-like protein E (PLP-E). The PLP-E receptor is present on megakaryocytes in pregnant mice, nonpregnant female mice, and male mice. Other known megakaryocytic cytokines do not share the PLP-E receptor, and thus the presence of this receptor in nonpregnant animals suggests that PLP-E may be expressed in tissues other than the placenta. Consistent with this prediction, PLP-E is produced in thrombocytopenic mouse bone marrow, primarily in granulocytes, but not in normal mouse bone marrow. Serum from thrombocytopenic mice, purified thrombopoietin or IL-6, or pregnancy can induce bone marrow cell expression of PLP-E. The induction of PLP-E gene expression in response to thrombocytopenia is physiologically significant, as injection of PLP-E into thrombocytopenic mice restores normal platelet levels with no effect on granulocytes, erythrocytes, and total white blood cell counts. We conclude that inducible expression of PLP-E in bone marrow is part of the mechanism of recovery from thrombocytopenia. These results also suggest a more general concept: that the endocrine program of pregnancy, which in mammals has evolved to support the intrauterine growth and development of the fetus, can also be harnessed to respond to pathophysiology.