之前研究證實，假懷孕及真懷孕大白鼠蛻膜細胞內的細胞質PKCα總量的減少是和調節子宮蛻膜細胞的生長有關。為了更進一步瞭解PKCα在人類子宮內膜組織和蛻膜組織中的表現，我們採用因子宮肌瘤手術而取得的18件正常子宮內膜檢體，和15件因早期妊娠合法終止懷孕的子宮蛻膜。採用RT-PCR的方法觀察子宮內膜及蛻膜中PKC異構物的含量，實驗結果發現，不同的PKC異構物在此兩種組織中各有不同的含量。我們使用免疫組織化學法和西方墨點法測量PKCα在人類子宮內膜和蛻膜中的表現量，結果顯示，PKCα在未懷孕的子宮內膜以及懷孕的子宮蛻膜中皆有表現。在子宮蛻膜中PKCα主要位於蛻膜細胞的細胞膜上，然而在子宮內膜的細胞膜上卻僅有少量染色的發現。我們進一步使用西方墨點法確認PKCα在人類蛻膜組織萃取液 (particulate fraction)中的表現量，結果發現PKCα在人類蛻膜組織萃取液中的表現量，明顯高於子宮內膜的表現量（P<0.05），但在兩者之細胞質（cytosolic fraction）中兩者並無明顯差異。接著採用PKCα的促進劑TPA及專一抑制劑Go6976分別加入此兩種組織中，並以明膠譜法（gelatin zymography）證實，若抑制PKCα的活性，結果也會抑制MMP-9的活性，但不影響MMP-2的活性。綜合上述結果發現，活化狀態且存在於人類蛻膜組織內的PKCα是屬於大量活化狀態，PKCα活化與MMP-9之間具相互關係。故PKCα可能參與調控人類子宮蛻膜的形成機制。 In our previous studies, we had found that the decreased cytosolic PKC α was associated with the modulation of decidual cell growth in pseudopregnancy and pregnancy rats. The aim of this study was to determine whether the distribution of cytosolic PKCα in human decidual tissue was the same as in the pseudopregnancy and pregnancy rats. Eighteen specimens of normal endometrial tissues from patients post uterine surgery （uterine myoma）, and fifteen decidual tissues from legal elective abortion. All of these tissues were sent for determining the mRNA content of PKC isoforms by using RT-PCR, the result showed that PKC isoforms within these tissues with different amounts. We also observed the expression of PKCα by IHC analysis and western Blot. The results showed that the expression of PKCα was observed in both endometrial and decidual tissues by immunohistochemical staining. In decidual tissue PKCα mainly located in membrane area, while that in endometrial tissue revealed little staining. Moreover, western blot also confirmed that the PKCα expression in particulate fraction in decidual tissues were significantly higher than that in endometrial tissues（P<0.05）, but in cytosolic fraction there were no difference. We further measured the expression of matrix metalloproteinase （MMP-2 and MMP-9）by using zymography after endometrium and decidua cells were treated by PKC activator（TPA） and PKCα specific inhibitor （G06976）, the results showed that the expression of MMP-9 was significantly decreased paralled with the inhibition of PKCα but MMP-2 did not show the same inhibitory results. These results indicated MMP-9 expression may be influenced by activated PKCα, and suggested that PKCα may be involved in the human uterine decidualization.
