Standaert M L, Cooper D R, Hernandez H, Arnold T P, Farese R V
Research Service, J. A. Haley V.A. Hospital, Tampa, Florida 33612.
Endocrinology. 1993 Feb;132(2):689-92. doi: 10.1210/endo.132.2.8425487.
In rat adipocytes, chronic incubation with 12-O-tetradecanoylphorbol-13-acetate (TPA) reduced immunoreactive protein kinase-C (PKC) beta, gamma, delta, and zeta isoforms by 40-60% and PKC alpha by 75%, but had little effect on PKC epsilon levels. In BC3H-1 myocytes, chronic TPA treatment had no effect on PKC beta, increased PKC zeta, and depleted PKC alpha. Acute treatment with insulin induced the translocation of PKC beta in the myocytes both before and after chronic TPA treatment, but had no acute effect on the alpha or zeta isoforms. In contrast, acute TPA treatment in the myocytes had little effect on PKC beta, but induced the rapid translocation of alpha and zeta. The differential effects of chronic TPA treatment on the down-regulation of PKC beta may explain why insulin continues to activate biological processes in TPA-treated BC3H-1 myocytes, but not in adipocytes.
在大鼠脂肪细胞中,用12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)进行长期孵育可使免疫反应性蛋白激酶C(PKC)的β、γ、δ和ζ亚型减少40% - 60%,PKCα减少75%,但对PKCε水平影响很小。在BC3H - 1肌细胞中,长期TPA处理对PKCβ没有影响,使PKCζ增加,并使PKCα减少。在长期TPA处理之前和之后,胰岛素急性处理均可诱导肌细胞中PKCβ的易位,但对α或ζ亚型没有急性影响。相反,肌细胞中的急性TPA处理对PKCβ影响很小,但诱导α和ζ快速易位。长期TPA处理对PKCβ下调的不同影响可能解释了为什么胰岛素能继续激活TPA处理过的BC3H - 1肌细胞中的生物学过程,但不能激活脂肪细胞中的生物学过程。