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首页> 外文期刊>Journal of Cellular Physiology >Transcriptional regulators of the ΔNp63: Their role in limbal epithelial cell proliferation
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Transcriptional regulators of the ΔNp63: Their role in limbal epithelial cell proliferation

机译：的转录监管机构ΔNp63:他们在缘的上皮细胞增殖中的作用

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摘要

The surface cells of corneal epithelium are regularly shed off and replaced by new cells that are derived from limbal epithelial stem cells (LESC). LESC are believed to reside in the basal layer of the limbal epithelium and are characterized with high expression levels of ΔNp63, a transcription factor (TF) which is believed to play roles in the regulation of LESC proliferation. In this study, we examined the transcriptional regulation of ΔNp63 in limbal epithelial cell. We employed DNA pull down assay followed by LC/MS analysis and cDNA microarray analysis to identify the TFs that were capable of binding to ΔNp63 promoter or were expressed at higher levels in limbus over cornea. The TFs thus selected were further examined for their in vivo ΔNp63 promoter binding by chromatin immunoprecipitation assay. We identified six putative TFs (PAX6, EGR1, CEBPB, JUN, ATF3, and ARID5B) through the aforementioned approaches. Among them, PAX6 and EGR1 were shown to promote the transcription of ΔNp63 and led to increased cell proliferation. In contrast, CEBPB and ATF3 appeared to exert little or no effect on ΔNp63 expression, however, their silencing suppressed cell proliferation. Although JUN exhibited low promoter-binding specificity, however, it affected ΔNp63 expression and limbal epithelial cell proliferation in ways similar to that of PAX6 and EGR1. Intriguingly, ARID5B was highly expressed in the limbal epithelial cell, however, its silencing by siRNA did not obviously affect the expression of ΔNp63, nor did it reduce cell proliferation of the limbal epithelial cell.
机译：角膜上皮的表层细胞经常脱落,取而代之的是新的细胞来自缘的上皮干细胞(LESC)。缘的上皮细胞层和表达水平高的特点ΔNp63,转录因子(TF)认为在LESC监管中发挥的作用扩散。转录调节ΔNp63缘的上皮细胞。其次是LC / MS分析和互补脱氧核糖核酸微阵列分析识别能力的助教绑定ΔNp63发起人或被表达更高的水平在角膜缘。选定的进一步检查他们的体内ΔNp63发起人通过染色质绑定免疫沉淀反应试验。假定的TFs (PAX6 EGR1 CEBPB,小君,ATF3,和通过上述方法ARID5B)。其中,PAX6 EGR1和促进的转录ΔNp63并导致增加细胞增殖。似乎产生很少或没有影响ΔNp63表情,然而,他们的沉默抑制细胞增殖。然而,promoter-binding特异性影响ΔNp63表达和缘的上皮细胞增殖的方式相似PAX6 EGR1。然而,缘的上皮细胞中表达,核的沉默并没有显著影响的表达ΔNp63,也没有减少细胞缘的上皮细胞的增殖。

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