Intracellular signaling and phasic myometrial contractions.
Intracellular signaling and phasic myometrial contractions.
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细胞内信号传导和阶段性子宫肌层收缩。
DOI：
10.1016/s1071-5576(98)00005-7
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Chien,EK
中科院分区：
文献类型：
--
作者：
Phillippe,M;Chien,EK
本文综述了最近报道的与子宫肌层组织发生时相收缩有关的细胞内信号转导机制。经典的子宫强直激动剂(包括催产素、去甲肾上腺素、加压素、乙酰胆碱和前列腺素[PGs])的细胞表面受体的存在已被很好地描述；所有这些都是跨七膜的G蛋白偶联受体。这些受体的占据，通过GQ和/或GI家族成员的异量滴定G蛋白，导致刺激磷脂酶C-β(PCL-β)亚型。非经典的子宫强直激动剂，如生长因子和细胞因子，也激活磷脂酰肌醇(PI)信号通路，在这种情况下，通过酪氨酸激酶受体介导的磷脂酶C-γ(PCL-γ)亚型的激活。最近的一些报道表明，子宫肌细胞中PI信号通路的激活导致细胞内钙振荡样现象的发生。这些胞内钙振荡似乎是由于内质网钙库随着细胞外钙的流入而排空和再充盈的接受性循环。内质网钙库的钙释放似乎是由肌醇敏感的三磷酸和兰诺定敏感的受体/通道介导的；这两种受体/通道的异构体都在子宫肌层组织中表达。总之，受体介导的PI信号通路的激活和胞浆钙振荡的产生似乎产生了间歇性的钙瞬变，导致了子宫肌层相性收缩的发展和维持。
This article reviews recently reported observations regarding the intracellular signal transduction mechanisms involved in the generation of phasic contractions occurring in myometrial tissue. The presence of cell surface receptors for classic uterotonic agonists (including oxytocin, norepinephrine, vasopressin, acetylcholine, and prostaglandins [PGs]) has been well described; all are seven-membrane-spanning, G protein-coupled receptors. Occupancy of these receptors, coupled through members of the Gq and/or Gi families of heterotrimetric G proteins, results in stimulation of the phospholipase C-β (PCL-β) isoforms. Nonclassic uterotonic agonists, such as growth factors and cytokines, also activate the phosphatidylinositol (PI)-signaling pathway, in this case through tyrosine kinase receptor-mediated activation of the phospholipase C-γ (PCL-γ) isoforms. Several recent reports have demonstrated that activation of the PI-signaling pathway in uterine myocytes results in the development of cytosolic calcium oscillation-like phenomena. These cytosolic calcium oscillations appear to arise from receptive cycles of emptying and refill of the endoplasmic reticulum calcium stores along with the influx of extracellular calcium. Calcium release from the endoplasmic reticulum calcium stores appears to be mediated by the inositol trisphosphate-sensitive and the ryanodine-sensitive receptor/channels; isoforms for both of these receptor/channels have been shown to be expressed in myometrial tissue. In summary, receptor-mediated activation of the PI-signaling pathway and the generation of cytosolic calcium oscillations appear to produce intermitten calcium transients that result in the development and maintenance of phasic myometrial contractions.