• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Archives of dermatological research. >Increased expression of p53 and p21 (Waf1/Cip1) in the lesional skin of bleomycin-induced scleroderma.
【24h】

Increased expression of p53 and p21 (Waf1/Cip1) in the lesional skin of bleomycin-induced scleroderma.

机译：在博来霉素诱导的硬皮病的病灶皮肤中p53和p21（Waf1 / Cip1）的表达增加。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Systemic sclerosis (SSc) is a connective tissue disorder characterized by excessive deposition of extracellular matrix in the affected skin as well as various internal organs, vascular injury and immune abnormality; however, the etiology of SSc remains still unknown. We previously established an experimental mouse model for scleroderma by repeated local injections of bleomycin, a DNA damaging agent. In this study, we examined the induction of apoptosis and the expression of p53, p21 (Waf1/Cip1), and proliferating cell nuclear antigen (PCNA) in the lesional skin following bleomycin exposure in this model. Dermal sclerosis was induced by alternate day's injections of bleomycin for 4 weeks. TUNEL assay showed that apoptotic cells began to appear at 1 week after bleomycin exposure, and were prominently detected at 3-4 weeks. Immunohistochemical examination showed increased expression of p53 and p21 mainly in the infiltrating mononuclear cells at 2 weeks after bleomycin treatment. Bleomycin treatment markedly enhanced PCNA expression at 1-2 weeks, mainly in mesenchyme, as compared with control phosphate buffered saline treatment. Reverse transcriptase-polymerase chain reaction analysis showed that the expression of p53 and p21 mRNA was concurrently upregulated at 1-2 weeks after bleomycin treatment. Taken together, coordinate increased levels of p53 and p21 preceded the maximal induction of apoptosis and dermal sclerosis. Our findings suggest that apoptotic processes are involved in the pathophysiology of bleomycin-induced scleroderma, which may be mediated, in part, by the upregulation of p53 and p21.
机译：系统性硬化症（SSc）是一种结缔组织疾病，其特征在于受影响的皮肤以及各种内部器官中细胞外基质的过多沉积，血管损伤和免疫异常;然而，SSc的病因仍然未知。我们之前通过反复局部注射博来霉素（一种DNA损伤剂）建立了硬皮病的小鼠实验模型。在这项研究中，我们检查了博莱霉素暴露后该病灶皮肤中凋亡的诱导以及p53，p21（Waf1 / Cip1）和增殖细胞核抗原（PCNA）的表达。隔日注射博来霉素持续4周可引起皮肤硬化。 TUNEL分析表明，博来霉素暴露后1周凋亡细胞开始出现，并在3-4周时被明显检测到。免疫组织化学检查显示，博来霉素处理后2周，p53和p21的表达主要在浸润的单个核细胞中增加。与对照磷酸盐缓冲盐水处理相比，博来霉素处理在1-2周时主要在间充质中显着增强PCNA表达。逆转录酶-聚合酶链反应分析表明，博来霉素处理后1-2周，p53和p21 mRNA的表达同时上调。两者合计，在最大程度地诱导凋亡和皮肤硬化之前，p53和p21水平的协调升高。我们的发现表明凋亡过程与博来霉素诱导的硬皮病的病理生理有关，这可能部分由p53和p21的上调介导。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号