Sanders J L, Stern P H
Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, Chicago, Illinois, USA.
J Bone Miner Res. 1996 Dec;11(12):1862-72. doi: 10.1002/jbmr.5650111206.
The protein kinase C (PKC) enzyme family consists of at least 11 isozymes in three classes, with characteristic tissue distributions. Phorbol esters activate and ultimately down-regulate phorbol-sensitive isozymes. PKC is a signal transducer in bone, and phorbol esters influence bone resorption. Little is known about specific PKC isozymes in this tissue, however. We describe here the expression and phorbol ester-induced down-regulation of PKC isozymes in osteoblasts. Normal mouse osteoblasts and seven osteoblastic cell lines (rat UMR-106, ROS 17/2.8, ROS 24/1, and human MG-63, G-292, SaOS-2, HOS-TE85) were screened for isozyme expression by Western immunoblotting using isozyme-specific anti-PKC antibodies. The conventional alpha and beta I isozymes, but not gamma, were present in each of the osteoblasts examined; PKC-beta II was detectable in all but the ROS 24/1 line. PKC-epsilon was expressed in all osteoblasts screened, but other novel PKCs, delta, eta, and theta, were detectable only in select lines. The atypical zeta and iota/lambda PKCs were in all osteoblasts examined. To determine the sensitivity of the isozymes to prolonged phorbol ester treatment, normal osteoblasts and the UMR-106 cell line were treated with vehicle or 1 microM phorbol 12, 13-dibutyrate (PDB) for 1, 3, 6, 12, 24, or 48 h, and Western blot analysis was performed. Normal and UMR-106 cells showed similar phorbol sensitivities; conventional (alpha, beta I) and novel (delta, epsilon, eta) isozymes were down-regulated by prolonged phorbol treatment but atypical isozymes were not. Down-regulation of all sensitive PKCs was detectable within 6 h of phorbol treatment; the novel delta and epsilon isozymes, however, showed more rapid and dramatic down-regulation than conventional isozymes. The observed down-regulation was dose-dependent (0.3-3 microM) and specific; 48 h treatment with the inactive phorbol, 4 alpha-phorbol 12,13-didecanoate (4 alpha-PDD), failed to down-regulate PDB-sensitive isozymes. The phorbol-induced down-regulation was also reversible; 24 h after withdrawing PDB, all phorbol-sensitive isozymes, except PKC-eta, had recovered at least partially. These studies, the first to characterize thoroughly PKC isozyme expression in osteoblastic cells from several species, demonstrate that osteoblasts have a characteristic PKC isozyme profile, including both phorbol ester-sensitive and -insensitive isozymes. The time course of down-regulation and the presence of phorbol-insensitive PKCs must be considered in interpreting the effects of phorbol esters on bone remodeling.
蛋白激酶C(PKC)酶家族由三个类别中至少11种同工酶组成,具有特征性的组织分布。佛波酯激活并最终下调对佛波敏感的同工酶。PKC是骨中的信号转导分子,佛波酯会影响骨吸收。然而,对于该组织中特定的PKC同工酶知之甚少。我们在此描述了成骨细胞中PKC同工酶的表达及佛波酯诱导的下调情况。通过使用同工酶特异性抗PKC抗体的Western免疫印迹法,对正常小鼠成骨细胞和七种成骨细胞系(大鼠UMR-106、ROS 17/2.8、ROS 24/1以及人MG-63、G-292、SaOS-2、HOS-TE85)进行同工酶表达筛选。在所检测的每个成骨细胞中均存在传统的α和βI同工酶,但γ不存在;除ROS 24/1细胞系外,在所有其他细胞系中均可检测到PKC-βII。PKC-ε在所有筛选的成骨细胞中均有表达,但其他新的PKC,即δ、η和θ,仅在特定细胞系中可检测到。非典型的ζ和ι/λ PKC存在于所有检测的成骨细胞中。为了确定同工酶对延长的佛波酯处理的敏感性,将正常成骨细胞和UMR-106细胞系用溶剂或1μM佛波12,13 - 二丁酸酯(PDB)处理1、3、6、12、24或48小时,然后进行Western印迹分析。正常细胞和UMR-106细胞表现出相似的佛波敏感性;延长的佛波处理可下调传统(α、βI)和新的(δ、ε、η)同工酶,但非典型同工酶不受影响。在佛波处理6小时内即可检测到所有敏感PKC的下调;然而,新的δ和ε同工酶比传统同工酶表现出更快且更显著的下调。观察到的下调是剂量依赖性的(0.3 - 3μM)且具有特异性;用无活性的佛波4α - 佛波12,13 - 二癸酸酯(4α - PDD)处理48小时未能下调对PDB敏感的同工酶。佛波诱导的下调也是可逆的;撤去PDB 24小时后,除PKC - η外,所有对佛波敏感的同工酶至少部分恢复。这些研究首次全面表征了来自多个物种的成骨细胞中PKC同工酶的表达,表明成骨细胞具有特征性的PKC同工酶谱,包括对佛波酯敏感和不敏感的同工酶。在解释佛波酯对骨重塑的影响时,必须考虑下调的时间进程以及对佛波不敏感的PKC的存在情况。