Smith R D
Department of Clinical Biochemistry, Addenbrooke's Hospital, Cambridge, UK.
Biochem Mol Biol Int. 1994 Aug;33(5):863-9.
Whereas direct activation of protein kinase C (PKC) by the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased the subsequent binding of 125I-labelled angiotensin II (125I-AII; 0.5 nM) to RIE-1 cells, ligand-mediated activation of the kinase via angiotensin II (AII), which activates the phosphoinositide (PI) pathway in these cells, had no effect. The apparent inability of AII to increase 125I-AII binding is unlikely to result from simultaneous, but opposing actions of AII on angiotensin receptor number and affinity since the peptide also had no effect on the saturation binding of 125I-AII (10 nM) to the cells. Since 125I-AII binding was unaffected both by AII pretreatment in PKC-depleted cells, and by the calcium ionophore, ionomycin, in PKC-replete cells, an attenuating action of AII (opposing any PKC-mediated increase) on 125I-AII binding mediated via the calcium limb of the PI pathway is also unlikely. Instead, the contrasting effects of AII and TPA on 125I-AII binding to RIE-1 cells appear to relate to the degree of PKC activation elicited by each agent.
佛波酯12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）对蛋白激酶C（PKC）的直接激活作用可增加随后125I标记的血管紧张素II（125I - AII；0.5 nM）与RIE - 1细胞的结合，而通过血管紧张素II（AII）对该激酶的配体介导激活（AII可激活这些细胞中的磷酸肌醇（PI）途径）则没有效果。AII无法增加125I - AII结合这一现象不太可能是由于AII对血管紧张素受体数量和亲和力同时产生相反作用导致的，因为该肽对125I - AII（10 nM）与细胞的饱和结合也没有影响。由于在PKC缺失的细胞中AII预处理以及在PKC充足的细胞中钙离子载体离子霉素对125I - AII结合均无影响，所以AII（对抗任何PKC介导的增加）对通过PI途径的钙分支介导的125I - AII结合产生减弱作用的可能性也不大。相反，AII和TPA对125I - AII与RIE - 1细胞结合的不同影响似乎与每种试剂引起的PKC激活程度有关。
