Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg, Würzburg, Germany.
Exp Hematol. 2013 Jan;41(1):91-101.e4. doi: 10.1016/j.exphem.2012.09.001. Epub 2012 Sep 11.
The cyclic nucleotides cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) regulate the activity of protein kinase A (PKA) and protein kinase G (PKG), respectively. This process helps maintain circulating platelets in a resting state. Here we studied the role of cAMP and cGMP in the regulation of megakaryocyte (MK) differentiation and platelet formation. Cultured, platelet-producing MKs were differentiated from fetal livers harvested from 13.5 days postcoital mouse embryos. MK development was accompanied by a dramatic increase in cAMP production and expression of soluble guanylate cyclase, PKG, and PKA as well as their downstream targets vasodilator-stimulated phosphoprotein (VASP) and MENA. Stimulation of prostaglandin E(1) receptor/adenylyl cyclase or soluble guanylate cyclase/PKG in cultured MKs increased VASP phosphorylation, indicating that these components share a common signaling pathway. To dissect out the role of cyclic nucleotides in MK differentiation, cAMP/PKA and cGMP/PKG signaling were alternately blocked in cultured MKs. Down-regulation of cAMP pathway effectors decreased MK numbers and ploidy. Notably, cGMP levels increased at the beginning of MK development and returned to basal levels in parallel with MK maturation. However, inhibition of cGMP pathway effectors had no effect on MK development. In addition, platelet release from mature MKs was enhanced by cGMP and inhibited by cAMP. Our data suggest that cAMP plays an important role in MK differentiation, while cAMP and cGMP have opposite effects on platelet production. Identifying the signaling pathways that underpin MK development and proplatelet formation will provide greater insights into thrombopoiesis and may potentially yield useful therapeutic targets.
环核苷酸环腺苷酸(cAMP)和环鸟苷酸(cGMP)分别调节蛋白激酶 A(PKA)和蛋白激酶 G(PKG)的活性。这一过程有助于维持循环血小板处于静止状态。在这里,我们研究了 cAMP 和 cGMP 在巨核细胞(MK)分化和血小板形成中的调节作用。从合胞体后 13.5 天的小鼠胚胎中收集胎肝,培养产生血小板的 MK 进行分化。MK 发育伴随着 cAMP 产生的急剧增加和可溶性鸟苷酸环化酶、PKG 和 PKA 的表达及其下游靶标血管扩张刺激磷蛋白(VASP)和 MENA。在培养的 MK 中刺激前列腺素 E1 受体/腺苷酸环化酶或可溶性鸟苷酸环化酶/PKG 会增加 VASP 磷酸化,表明这些成分共享一个共同的信号通路。为了剖析循环核苷酸在 MK 分化中的作用,交替阻断培养的 MK 中的 cAMP/PKA 和 cGMP/PKG 信号通路。下调 cAMP 通路效应物会减少 MK 的数量和倍性。值得注意的是,cGMP 水平在 MK 发育开始时升高,并在与 MK 成熟平行时恢复到基础水平。然而,抑制 cGMP 通路效应物对 MK 发育没有影响。此外,cGMP 增强成熟 MK 中血小板的释放,并抑制 cAMP。我们的数据表明 cAMP 在 MK 分化中起重要作用,而 cAMP 和 cGMP 对血小板生成有相反的影响。确定支持 MK 发育和原血小板形成的信号通路将提供对血栓形成的更深入了解,并可能产生有用的治疗靶点。