Chen T T, Wu R L, Castro-Munozledo F, Sun T T
Department of Pharmacology, New York University School of Medicine, New York 10016, USA.
Mol Cell Biol. 1997 Jun;17(6):3056-64. doi: 10.1128/MCB.17.6.3056.
Rabbit corneal epithelial cells cultured in the presence of 3T3 feeder cells undergo biochemical differentiation, as evidenced by their initial expression of K5 and K14 keratins characteristic of basal keratinocytes, followed by the subsequent expression of K3 and K12 keratin markers of corneal epithelial differentiation. Previous data established that mutations of an Sp1 site in a DNA element, E, that contains overlapping Sp1 and AP-2 motifs reduce K3 gene promoter activity by 70% in transfection assays. We show here that Sp1 activates while AP-2 represses the K3 promoter. Although undifferentiated corneal epithelial basal cells express equal amounts of Sp1 and AP-2 DNA-binding activities, the differentiated cells down-regulate their Sp1 activity slightly but their AP-2 activity drastically, thus resulting in a six- to sevenfold increase in the Sp1/AP-2 ratio. This change coincides with the activation and suppression of the differentiation-related K3 gene and the basal cell-related K14 keratin gene, respectively. In addition, we show that polyamines, which are present in a high concentration in proliferating basal keratinocytes, can inhibit the binding of Sp1 to its cognate binding motif but not that of AP-2. These results suggest that the relatively low Sp1/AP-2 ratio as well as the polyamine-mediated inhibition of Sp1 binding to the E motif may account, in part, for the suppression of the K3 gene in corneal epithelial basal cells, while the elevated Sp1/AP-2 ratio may be involved in activating the K3 gene in differentiated corneal epithelial cells. Coupled with the previous demonstration that AP-2 activates the K14 gene in basal cells, the switch of the Sp1/AP-2 ratio during corneal epithelial differentiation may play a role in the reciprocal expression of the K3 and K14 genes in the basal and suprabasal cell layers.
在3T3饲养细胞存在的情况下培养的兔角膜上皮细胞会发生生化分化,这可通过它们最初表达基底角质形成细胞特有的K5和K14角蛋白得以证明,随后会表达角膜上皮分化的K3和K12角蛋白标志物。先前的数据表明,在一个含有重叠Sp1和AP-2基序的DNA元件E中,Sp1位点的突变在转染试验中会使K3基因启动子活性降低70%。我们在此表明,Sp1激活而AP-2抑制K3启动子。尽管未分化的角膜上皮基底细胞表达等量的Sp1和AP-2 DNA结合活性,但分化细胞会轻微下调其Sp1活性,而大幅下调其AP-2活性,从而导致Sp1/AP-2比值增加6至7倍。这种变化分别与分化相关的K3基因和基底细胞相关的K14角蛋白基因的激活和抑制相吻合。此外,我们表明,在增殖的基底角质形成细胞中高浓度存在的多胺可抑制Sp1与其同源结合基序的结合,但不会抑制AP-2的结合。这些结果表明,相对较低的Sp1/AP-2比值以及多胺介导的对Sp1与E基序结合的抑制可能部分解释了角膜上皮基底细胞中K3基因的抑制,而升高的Sp1/AP-2比值可能参与激活分化的角膜上皮细胞中的K3基因。再加上先前证明AP-2在基底细胞中激活K14基因,角膜上皮分化过程中Sp1/AP-2比值的转换可能在基底和基底上层细胞层中K3和K14基因的相互表达中起作用。