正常、糖尿病及胰岛素治疗的糖尿病大鼠前列腺上皮细胞中的蛋白激酶C同工酶

Protein kinase C isozymes in prostatic epithelial cells from normal, diabetic and insulin-treated diabetic rats.

Garcia-Paramio P L, Carmena M J, Guijarro L G, Prieto J C

Unidad de Neuroendocrinologia Molecular, Departamento de Bioquimica y Biologia Molecular, Universidad de Alcala, Spain.

Gen Pharmacol. 1995 Dec;26(8):1673-8. doi: 10.1016/0306-3623(95)00035-6.

Abstract

Immunoblot experiments in rat prostatic epithelium using a non-selective antibody against protein kinase C (PKC) allowed to detect three PKC subspecies of 87.5, 55.5 and 34.6 kDa that showed higher, similar and lower immunoreactivity in the membrane than in the cytosolic compartment, respectively. 2. Specific monoclonal antisera revealed that the PKC-gamma isozyme is not expressed in the rat prostatic epithelium, whereas the PKC-beta isozyme was noted only in the cytosolic fraction showing an apparent molecular weight of 75.5 kDa. 3. Induction of diabetes by streptozotocin led to modifications in the expression of PKC isozymes so that the immunoreactivities of the 87.5- and 55.5-kDa PKC forms decreased in both cytosolic and membrane subcellular fractions to different extents. 4. The most important decrease was that of the 55.5-kDa PKC form in cytosol that returned to control values by insulin therapy, whereas PKC-beta suffered also some decrease in diabetes and increased again with insulin treatment.

摘要

在大鼠前列腺上皮中使用针对蛋白激酶C（PKC）的非选择性抗体进行免疫印迹实验，可检测到三种PKC亚型，分子量分别为87.5、55.5和34.6 kDa，它们在膜中的免疫反应性分别高于、相似于和低于胞质区室。2. 特异性单克隆抗血清显示，PKC-γ同工酶在大鼠前列腺上皮中不表达，而PKC-β同工酶仅在胞质部分被检测到，其表观分子量为75.5 kDa。3. 链脲佐菌素诱导的糖尿病导致PKC同工酶表达发生改变，使得87.5 kDa和55.5 kDa的PKC形式在胞质和膜亚细胞部分的免疫反应性均有不同程度降低。4. 最重要的降低是胞质中55.5 kDa的PKC形式，胰岛素治疗后恢复至对照值，而PKC-β在糖尿病时也有所降低，胰岛素治疗后再次升高。