Roles and mechanisms of TRPC3 and the PLCγ/PKC/CPI-17 signaling pathway in regulating parturition.
Roles and mechanisms of TRPC3 and the PLCγ/PKC/CPI-17 signaling pathway in regulating parturition.
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TRPC3和PLCγ/PKC/CPI-17信号传导途径在调节分娩中的作用和机制。
DOI：
10.3892/mmr.2017.7998
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发表时间：
2018-01
影响因子：
3.4
通讯作者：
Liu C
中科院分区：
文献类型：
--
作者：
Chen J;Zheng D;Cui H;Liu S;Zhang L;Liu C
本研究旨在探讨磷脂酶C (PLC)γ/蛋白激酶C (PKC)/C激酶活化蛋白磷酸酶-1 （CPI-17）信号通路在分娩过程中子宫平滑肌中的作用。子宫组织样本采集于因早产、足月分娩伴阵痛、足月分娩无阵痛的孕妇，以及因宫颈上皮内瘤变III型手术的非妊娠对照组。采用免疫组织化学和western blotting方法评估TRPC3水平与分娩的关系以及钙离子通道的影响。此外，利用妊娠小鼠研究子宫典型瞬时受体电位3 （TRPC3）表达对分娩触发机制和PLCγ/PKC/CPI-17信号通路的影响。培养妊娠小鼠子宫平滑肌细胞，沉默TRPC3和不沉默TRPC3，测定妊娠小鼠子宫平滑肌细胞中TRPC3通路上下游因子PLCγ、PKC和pci -17的表达水平，为早产的预防和治疗提供理论依据。在早产和足月未分娩患者组中，与未妊娠组相比，mSMCs中TRPC3基因表达明显过表达（P<0.05）；而TRPC3表达在足月伴产组未升高，与未妊娠组比较差异无统计学意义（P < 0.05）。妊娠期间，与未妊娠对照组相比，早产组和足月分娩组的mSMCs中Cav1.2、Cav3.1和Cav3.2基因表达水平显著升高（P<0.05），而足月未分娩组Cav1.2、Cav3.1和Cav3.2基因表达水平无显著升高。TRPC3水平在早产儿组最高，Cav1.2、Cav3.1、Cav3.2水平在足月伴产组最高。在早产、lps处理的早产儿和足月组中，TRPC3、MAPK、ERK1/2、P-ERK、Cav3.2、Cav3.1和Cav1.2的表达水平均高于未受精组。lps处理早产儿组TRPC3、MAPK、ERK1/2、P-ERK、Cav3.2、Cav3.1、Cav1.2水平较早产儿组升高。此外，将小干扰TRPC3 （siTRPC3）转染细胞后，我们发现，与未转染LPS处理的对照组相比，LPS siTRPC3组TRPC3、PLCγ、PKC、CPI-17、P-CPI-17、Cav1.2、Cav3.1和Cav3.2的表达水平较低。
The aim of the current study was to investigate the role of phospholipase C (PLC)γ/protein kinase C (PKC)/C-kinase-activated protein phosphatase-1 (CPI-17) signaling pathways in uterine smooth muscle during parturition. Samples of uterine tissue were collected from pregnant patients who underwent a caesarean section for preterm delivery, full-term delivery with labor onset, full-term delivery without labor onset, and from a non-pregnant control group undergoing surgery for cervical intraepithelial neoplasia III. Immunohistochemistry, and western blotting were used to assess the association between TRPC3 levels and parturition and the influence of calcium ion channels. In addition, pregnant mice were used to explore the effect of uterine canonical transient receptor potential 3 (TRPC3) expression on the parturition-triggering mechanism and PLCγ/PKC/CPI-17 signaling pathways. Pregnant mouse uterine smooth muscle cells were cultivated, with and without TRPC3 silencing, and the expression levels of PLCγ, PKC and CPI-17, the upstream and downstream factors of the TRPC3 pathway, were measured in pregnant mouse uterine smooth muscle cells, in order to provide a theoretical basis for the prevention and treatment of premature labor. In the preterm and full-term without labor onset patient groups, the TRPC3 gene expression in the mSMCs was significantly overexpressed when compared with the non-pregnant group (P<0.05); however, TRPC3 expression was not elevated in the full-term with labor onset group, exhibiting no significant difference compared with the non-pregnant group (P>0.05). During pregnancy, compared with the non-pregnant controls, Cav1.2, Cav3.1 and Cav3.2 gene expression levels were markedly increased (P<0.05) in mSMCs from the preterm delivery group and the full-term with labor onset group, however were non-significantly increased in the full-term without labor onset group. The level of TRPC3 was highest in the preterm group, while the levels of Cav1.2, Cav3.1 and Cav3.2 were highest in the full-term with labor onset group. In the preterm, LPS-treated preterm and full-term groups, TRPC3, MAPK, ERK1/2, P-ERK, Cav3.2, Cav3.1 and Cav1.2 were all expressed at higher levels than in the unfertilized group. In the LPS-treated preterm group, the levels of TRPC3, MAPK, ERK1/2, P-ERK, Cav3.2, Cav3.1 and Cav1.2 were increased compared with the preterm group. Furthermore, following transfection of small interfering TRPC3 (siTRPC3) into cells, it was demonstrated that the levels of TRPC3, PLCγ, PKC, CPI-17, P-CPI-17, Cav1.2, Cav3.1 and Cav3.2 expression were lower in the LPS siTRPC3 group when compared with that of the LPS-treated untransfected control group.
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DOI：
10.1152/ajplung.00398.2003
发表时间：
2004-11-01
影响因子：
4.9
作者：
Kolosova, IA;Ma, SF;Verin, AD
通讯作者：
Verin, AD
影响因子：
0.9
作者：
Ijaiya, Munir'deen A.;Adesina, Kike T.;Isiaka-Lawal, Salamat
通讯作者：
Isiaka-Lawal, Salamat
DOI：
10.1016/j.bbrc.2004.02.014
发表时间：
2004-03-26
影响因子：
3.1
作者：
Zemlickova, E;Johannes, FJ;Dubois, T
通讯作者：
Dubois, T
影响因子：
4.1
作者：
Murthy, KS;Zhou, HP;Makhlouf, GM
通讯作者：
Makhlouf, GM
影响因子：
5.4
作者：
Ohno, Yasumasa;Terauchi, Mikio;Saito, Shigeru
通讯作者：
Saito, Shigeru