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首页> 外文期刊>The Journal of investigative dermatology. >Impaired skin regeneration and remodeling after cutaneous injury and chemically induced hyperplasia in taps-transgenic mice.
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Impaired skin regeneration and remodeling after cutaneous injury and chemically induced hyperplasia in taps-transgenic mice.

机译：自来水转基因小鼠皮肤损伤和化学诱导的增生后皮肤再生和重塑受损。

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摘要

Recently, we identified an AP-1-dependent target gene in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated mouse back skin, which encodes a retroviral-like aspartic proteinase (Taps/Asprv1). Taps expression was detected almost exclusively in stratified epithelia of mouse embryos and adult tissues, and enhanced protein levels were present in several non-neoplastic human skin disorders, implicating a crucial role for differentiation and homeostasis of multilayered epithelia. Here, we generated a mouse model in which Taps transgene expression is under the control of the human ubiquitin C promoter (UBC-Taps). Although no obvious phenotype was observed in normal skin development and homeostasis, these mice showed a significant delay in cutaneous wound closure compared with control animals. Shortly after re-epithelialization, we found an increase in keratinocytes in the stratum granulosum, which express Filaggrin, a late differentiation marker. A hypergranulosum-like phenotype with increased numbers of Filaggrin-positive keratinocytes was also observed in UBC-Taps mice after administration of TPA. In summary, these data show that aberrant Taps expression causes impaired skin regeneration and skin remodeling after cutaneous injury and chemically induced hyperplasia.
机译：最近，我们在12-O-十四烷酰phorbol-13-乙酸酯（TPA）处理的小鼠背部皮肤中鉴定了AP-1依赖性靶基因，该基因编码逆转录病毒样天冬氨酸蛋白酶（Taps / Asprv1）。 Taps的表达几乎仅在小鼠胚胎和成年组织的分层上皮中检测到，并且在几种非肿瘤性人类皮肤病中存在增强的蛋白质水平，这暗示了多层上皮的分化和体内平衡的关键作用。在这里，我们生成了一个小鼠模型，其中Taps转基因表达处于人泛素C启动子（UBC-Taps）的控制之下。尽管在正常的皮肤发育和体内平衡中未观察到明显的表型，但与对照动物相比，这些小鼠的皮肤伤口闭合明显延迟。重新上皮化后不久，我们发现颗粒层中的角质形成细胞增加，表达晚期分化标记物Filaggrin。给予TPA后，在UBC-Taps小鼠中还观察到了具有增加的Filaggrin阳性角质形成细胞数量的超颗粒状表型。总之，这些数据表明，Taps的异常表达会导致皮肤再生和化学诱导的增生后受损的皮肤再生和皮肤重塑。

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