Adenosine receptor‐like molecules and related signaling transduction pathways regulate hemocyte adhesion in abalone (Haliotis diversicolor)

Abstract

Blood cell adhesion is the very first step to perform those cellular defenses like phagocytosis and encapsulation. We report here that caffeine and other adenosine receptor (AdoR) agonists influenced hemocyte adhesion in abalones (Haliotis diversicolor). Caffeine (AdoR antagonists), CHA, and R-PIA (both AdoA1R agonists), as well as IB-MECA (AdoA3R agonist) can inhibit the hemocyte adhesion while CGS21680 (AdoA2AR agonist) activates hemocyte adhesion. The adhesion inhibition result of adenosine treatment is similar to AdoA1R agonists. Adenosine receptors have been recognized as the members of G-protein coupled receptor family, and the major intracellular signaling transduction pathways downstream the receptors are cAMP-PKA pathway and PLC. In this study, the treatment of dbcAMP, PMA (PKC activator), or A23187 (calcium ionophore) that increased the hemocyte adhesion. Although AdoA1R agonists decreased the intracellular cAMP concentration, additional loaded dbcAMP could not recover the inhibitory effect of AdoA1R agonists on hemocyte adhesion. In addition, either PLC inhibitor (U73122) or PI3K inhibitors (wortmannin or LY294002) could inhibit the hemocyte adhesion. Together, the results suggest there are adenosine receptors or adenosine receptor-like molecules on abalone hemocytes which are involved in abalone hemocyte adhesion. The hemocyte adhesion that inhibited by activation of AdoA1R should be regulated by signaling pathways like PLC-PKC pathway or PI3K, and the cAMP-PKA pathway is also involved, but may not be the major signaling pathway that control hemocyte adhesion. Abbreviations AdoR, adenosine receptor; AdoA1R, adenosine A1 receptor; AdoA2AR, adenosine A2A receptor; AdoA3R, adenosine A3 receptor