| Abstract: | 先前我們應用假孕鼠研究初步結果顯示,蛻膜瘤組織形成期間與對照之子宮組織比較時,細胞質的PKC活性在統計上有顯著減少(3),並且發現PKC異構體(.alpha.,.delta.,.zeta.,.lambda.,.iota.)與假孕鼠之子宮內膜增殖有密切關聯(4,5),推論PKC異構體的表現可能伴隨蛻膜瘤組織生長的調節。做本實驗計畫擬進一步深入應用體外培養模式探討人類子宮內膜基質細胞(Endometrial stromal cell)增殖形成蛻膜細胞期間PKC所扮演的角色,以進一步了解蛻膜細胞形成之機制。結果顯示經由Progesterone處理的人類子宮內膜基質細胞分化成蛻膜細胞後,細胞質的PKC.alpha.含量有明顯下降的現象,這種現象可能與活化下降調節作用(Activation and down-regulation)有關。另外利用Zymopraphy的檢測MMP分泌的情形,發現在Progesterone處理組中MMP-2的分泌也比對照組的細胞少。可見蛻膜細胞內MMP-2的分泌可能與PKC的表現有關。
Our previous data showed that the activity of cytosolic PKC was significantly decreased in the deciduomata as comparing with that in the control uterine tissue (5), and that the various expression of PKC isoforms (.alpha., .delta., .zeta., .iota. and .lambda.) were observed in the trauma-induced decidualization. It is suggested that the various expression of PKC isoforms were involved in the modulation of the development of deciduomata. In this study, we established in vitro system for confirming PKC commitment. We separated epithelial and stromal cell cultures form normal human endometrium to test the expression of PKC isoforms in the decidualization. The results showed that the decreased expression of PKC.alpha. was observed in the progesterone-treated group as compared to the control group. Moreover, the decreased secrection of MMP-2 was also detected in the progesterone-treated group. Thus, we suggested that the decreased expression of PKC.alpha. may be correlated with the reduction of the MMP-2 secrection in the decidualization of human endometrial stromal cell. |
