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首页> 外文期刊>Journal of applied toxicology >Gene expression changes associated with altered growth and differentiation in benzo(a)pyrene or arsenic exposed normal human epidermal keratinocytes.
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Gene expression changes associated with altered growth and differentiation in benzo(a)pyrene or arsenic exposed normal human epidermal keratinocytes.

机译：基因表达变化与苯并（a）or或砷暴露的正常人表皮角质形成细胞中生长和分化的改变有关。

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摘要

Both arsenic and benzo[a]pyrene (BaP) inhibit terminal differentiation and alter growth potential in normal human epidermal keratinocytes (NHEK) in vitro. To identify molecular alterations that may be involved in these cellular processes, microarray analysis was carried out on NHEK treated with BaP or arsenic. The gene expression microarray results measuring mRNA levels were as follows: (1) in total, the expression of 85 genes was induced and 17 genes was suppressed by 2.0 microm BaP. (2) Arsenic at an equitoxic dose (5.0 microm) induced the expression of 106 and suppressed 15 genes. Quantitative real-time RT-PCR was used subsequently to confirm microarray findings on selected genes involved in keratinocyte growth and differentiation pathways. These studies confirmed increased mRNA levels in NHEK by BaP of alpha-integrin binding protein 63 (AIBP63) (2.48-fold), retinoic acid- and interferon-inducible protein (IFIT5) (2.74-fold), interleukin-1 alpha (IL1A) (2.64-fold), interleukin-1 beta (IL1B) (2.84-fold) and Ras guanyl releasing protein 1 (RASGRP1) (3.14-fold). Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold). Collectively, these results indicate that these chemicals target different genes and molecular pathways involved in the regulatory processes controlling NHEK proliferation and differentiation. Mechanistic studies with a subset of genes may allow the correlation of alterations in these molecular markers with chemical-specific blocks to differentiation in NHEK.
机译：砷和苯并[a]（（BaP）均可在体外抑制正常人表皮角质形成细胞（NHEK）的终末分化并改变其生长潜力。为了鉴定可能与这些细胞过程有关的分子变化，对用BaP或砷处理的NHEK进行了微阵列分析。测定mRNA水平的基因表达微阵列结果如下：（1）总共用2.0μmBaP诱导了85个基因的表达并抑制了17个基因。 （2）等毒性剂量（5.0微米）的砷诱导106的表达并抑制15个基因。随后使用定量实时RT-PCR来确认关于参与角质形成细胞生长和分化途径的选定基因的微阵列发现。这些研究证实，α-整联蛋白结合蛋白63（AIBP63）（2.48倍），视黄酸和干扰素诱导蛋白（IFIT5）（2.74倍），白介素-1α（IL1A）的BaP可以增加NHEK中的mRNA水平。 （2.64倍），白介素1β（IL1B）（2.84倍）和拉斯鸟嘌呤释放蛋白1（RASGRP1）（3.14倍）。实时RT-PCR证实砷增加了以下基因的mRNA水平：视网膜母细胞瘤1（RB1）（5.4倍），视网膜母细胞瘤结合蛋白1（ARID4A）（6.8倍），转化生长因子β刺激的蛋白（ TSC22D1）（6.84倍），MAX结合蛋白（MNT）（2.44倍）和RAD50（4.24倍）。总的来说，这些结果表明，这些化学药品的目标是控制NHEK增殖和分化的调控过程中涉及的不同基因和分子途径。用基因子集进行的机理研究可能使这些分子标记的变化与化学特异性嵌段与NHEK的分化相关。

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