Review: Leptin gene expression in the placenta - Regulation of a key hormone in trophoblast proliferation and survival
Review: Leptin gene expression in the placenta - Regulation of a key hormone in trophoblast proliferation and survival
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DOI：
10.1016/j.placenta.2011.01.004
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发表时间：
2011-03-01
期刊：
影响因子：
3.8
通讯作者：
Varone, C. L.
中科院分区：
文献类型：
--
作者：
Maymo, J. L.;Perez-Perez, A.;Varone, C. L.
瘦素是一种16000 mW的蛋白质，最初被描述为脂肪细胞衍生的信号分子，用于中央控制新陈代谢。然而，瘦素在生殖和妊娠中的多效性作用已被发现。瘦素基因在胎盘中表达，促进滋养层细胞的增殖和存活。对已知由瘦素受体触发的主要信号通路的研究表明，瘦素刺激胎盘细胞中的JAK/STAT、MAPK和PI3K通路。瘦素也在胎盘中发挥抗细胞凋亡的作用，这种作用是通过MAPK途径介导的。此外，瘦素通过PI3K和MAPK途径激活翻译机制，从而刺激蛋白质合成。胎盘中瘦素的表达受到高度调节，这表明某些关键的妊娠分子参与了这种调节。人绒毛膜促性腺激素(HCG)是一种重要的生殖激素，它诱导滋养层细胞表达瘦素，这种作用涉及MAPK信号转导通路。此外，环核苷酸cAMP对人滋养层细胞的功能有深远的影响，它也刺激瘦素的表达，这种作用似乎是通过PKA和MAPK信号通路之间的串扰来实现的。雌激素在生殖过程中起着核心作用。17β-雌二醇通过基因组和非基因组作用上调胎盘细胞中瘦素的表达，可能是通过雌激素受体-α与MAPK和PI3K信号转导通路之间的串扰。综上所述，这些发现有助于更好地了解瘦素在人胎盘滋养层细胞中的功能和表达的调控机制，并进一步支持瘦素在生殖生物学中的重要性。(C)2011年，由IFPA和爱思唯尔有限公司出版。
Leptin is a 16000 MW protein originally described as an adipocyte-derived signaling molecule for the central control of metabolism. However, pleiotropic effects of leptin have been identified in reproduction and pregnancy. The leptin gene is expressed in placenta, where leptin promotes proliferation and survival of trophoblast cells. Study of the major signaling pathways known to be triggered by leptin receptor has revealed that leptin stimulates JAK/STAT, MAPK and PI3K pathways in placental cells. Leptin also exerts an antiapoptotic action in placenta and this effect is mediated by the MAPK pathway. Moreover, leptin stimulates protein synthesis by activating the translational machinery via both PI3K and MAPK pathways. Expression of leptin in placenta is highly regulated, suggesting that certain key pregnancy molecules participate in such regulation. An important hormone in reproduction, hCG, induces leptin expression in trophoblast cells and this effect involves the MAPK signal transduction pathway. Moreover, the cyclic nucleotide cAMP, which has profound actions upon human trophoblast function, also stimulates leptin expression and this effect seems to be mediated by crosstalk between the PKA and MAPK signaling pathways. Estrogens play a central role in reproduction. 17 beta-estradiol upregulates leptin expression in placental cells through genomic and non-genomic actions, probably via crosstalk between estrogen receptor-alpha and the MAPK and PI3K signal transduction pathways. Taken together these findings give a better understanding of the function of leptin and the regulatory mechanisms of leptin expression in human placental trophoblast and further support the importance of leptin in the biology of reproduction. (C) 2011 Published by IFPA and Elsevier Ltd.