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前列腺素F2α刺激子宫肌层阶段性收缩的细胞内机制。

Intracellular mechanisms underlying prostaglandin F2alpha-stimulated phasic myometrial contractions.

作者信息

Phillippe M, Saunders T, Basa A

机构信息

Department of Obstetrics and Gynecology, University of Chicago, Illinois 60637, USA.

出版信息

Am J Physiol. 1997 Oct;273(4):E665-73. doi: 10.1152/ajpendo.1997.273.4.E665.

Abstract

These studies sought to test the hypothesis that prostaglandin F2alpha (PGF2alpha)-stimulated phasic myometrial contractions are characterized by the activation of the phosphatidylinositol-signaling pathway resulting in the generation of cytosolic calcium oscillations. For the experiments described in this report rat myometrial tissue was used, after the tissue was loaded with fura 2, to perform cytosolic calcium imaging studies and to perform computer-digitalized in vitro isometric contraction studies. Consistent with the above hypothesis, the cytosolic calcium-imaging studies demonstrated PGF2alpha-stimulated cytosolic calcium oscillations occurring simultaneously with phasic contractions. The in vitro isometric contraction studies confirmed that previously reported inhibitors of the phosphatidylinositol-signaling pathway and cytosolic calcium oscillation mechanisms resulted in significant inhibition of PGF2alpha-stimulated phasic myometrial contractions. In summary, these studies have provided substantial support for the hypothesis that PGF2alpha-stimulated phasic myometrial contractions are generated by intracellular signaling mechanisms involving activation of the phosphatidylinositol-signaling pathway and the production of cytosolic calcium oscillation-like phenomena.

摘要

这些研究旨在验证以下假设

前列腺素F2α(PGF2α)刺激的子宫肌层阶段性收缩的特征是磷脂酰肌醇信号通路的激活,从而导致胞质钙振荡的产生。对于本报告中描述的实验,在将大鼠子宫肌层组织用fura 2加载后,用于进行胞质钙成像研究和计算机数字化体外等长收缩研究。与上述假设一致,胞质钙成像研究表明,PGF2α刺激的胞质钙振荡与阶段性收缩同时发生。体外等长收缩研究证实,先前报道的磷脂酰肌醇信号通路和胞质钙振荡机制的抑制剂可显著抑制PGF2α刺激的子宫肌层阶段性收缩。总之,这些研究为以下假设提供了大量支持:PGF2α刺激的子宫肌层阶段性收缩是由涉及磷脂酰肌醇信号通路激活和胞质钙振荡样现象产生的细胞内信号机制所引发的。

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