依據本實驗以下幾點發現:一、細胞附著的過程中,細胞內cAMP的量會逐漸下降;二、加入cAMP analog會抑制細胞的附著;三、Protein Kinase A受到抑制物作用後,細胞的附著率反而明顯的提高;四、細胞附著的時間越長,PKA的活性會隨著時間的增加而降低。證實PKA這條訊息傳導途徑參與並調控九孔血液細胞的附著。然而另一條由cAMP所調控的Epac訊息傳導途徑則由於對Epac具有專一性的cAMP analog對細胞的附著卻沒有任何影響,因此應與此細胞附著無關。另外,實驗亦發現,加入RGD肽胜會抑制細胞的附著,推測細胞在附著的時候是經由細胞膜上的細胞附著分子integrin與細胞間質中的蛋白質相互作用,來調節細胞附著。
The adhesion of hemocytes plays an important role in the innate immunity of abalones. According to the results from this study, several conclusions were drawn about the role of PKA (protein kinase A) in the adhesion of abalone hemocytes. First, upon cell adhesion, the amount of cAMP decreased in hemocytes. Second, elevation of cAMP levels inhibited cell adhesion. Third, cell adhesion was enhanced by the PKA inhibitor KT5720. Fourth, PKA activity decreased upon adhesion was in a time-dependent manner. Therefore, these results strongly suggested that the adhesion of abalone hemocyte is regulated by PKA and the subsequent signal transduction pathway. However, another cAMP-mediated protein Epac was not involved in the regulation of the adhesion of hemocytes. Besides, since RGD peptides affected the cell adhesion suggested that the adhesion of abalone hemocytes was mediated by the interactions between integrins and fibronection.