Ohba M, Ishino K, Kashiwagi M, Kawabe S, Chida K, Huh N H, Kuroki T
Department of Microbiology, School of Pharmaceutical Sciences, Showa University, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Mol Cell Biol. 1998 Sep;18(9):5199-207. doi: 10.1128/MCB.18.9.5199.
Protein kinase C (PKC) plays a crucial role(s) in regulation of growth and differentiation of cells. In the present study, we examined possible roles of the alpha, delta, eta, and zeta isoforms of PKC in squamous differentiation by overexpressing these genes in normal human keratinocytes. Because of the difficulty of introducing foreign genes into keratinocytes, we used an adenovirus vector system, Ax, which allows expression of these genes at a high level in almost all the cells infected for at least 72 h. Increased kinase activity was demonstrated in the cells overexpressing the alpha, delta, and eta isoforms. Overexpression of the eta isoform inhibited the growth of keratinocytes of humans and mice in a dose (multiplicity of infection [MOI])-dependent manner, leading to G1 arrest. The eta-overexpressing cells became enlarged and flattened, showing squamous cell phenotypes. Expression and activity of transglutaminase 1, a key enzyme of squamous cell differentiation, were induced in the eta-overexpressing cells in dose (MOI)- and time-dependent manners. The inhibition of growth and the induction of transglutaminase 1 activity were found only in the cells that express the eta isoform endogenously, i.e., in human and mouse keratinocytes but not in human and mouse fibroblasts or COS1 cells. A dominant-negative eta isoform counteracted the induction of transglutaminase 1 by differentiation inducers such as a phorbol ester, 1alpha,25-dihydroxyvitamin D3, and a high concentration of Ca2+. Among the isoforms examined, the delta isoform also inhibited the growth of keratinocytes and induced transglutaminase 1, but the alpha and zeta isoforms did not. These findings indicate that the eta and delta isoforms of PKC are involved crucially in squamous cell differentiation.
蛋白激酶C(PKC)在细胞生长和分化的调控中起着关键作用。在本研究中,我们通过在正常人角质形成细胞中过表达这些基因,研究了PKC的α、δ、η和ζ亚型在鳞状分化中的可能作用。由于将外源基因导入角质形成细胞存在困难,我们使用了腺病毒载体系统Ax,该系统可使这些基因在几乎所有感染至少72小时的细胞中高水平表达。在过表达α、δ和η亚型的细胞中证实了激酶活性增加。η亚型的过表达以剂量(感染复数[MOI])依赖的方式抑制人和小鼠角质形成细胞的生长,导致G1期停滞。过表达η的细胞变得增大且扁平,呈现鳞状细胞表型。转谷氨酰胺酶1(鳞状细胞分化的关键酶)的表达和活性在过表达η的细胞中以剂量(MOI)和时间依赖的方式被诱导。仅在内在表达η亚型的细胞中,即人和小鼠角质形成细胞中,而非人和小鼠成纤维细胞或COS1细胞中,发现了生长抑制和转谷氨酰胺酶1活性的诱导。一种显性负性η亚型抵消了佛波酯、1α,25 - 二羟基维生素D3和高浓度Ca2 +等分化诱导剂对转谷氨酰胺酶1的诱导作用。在所检测的亚型中,δ亚型也抑制角质形成细胞的生长并诱导转谷氨酰胺酶1,但α和ζ亚型则没有。这些发现表明,PKC的η和δ亚型在鳞状细胞分化中起关键作用。