Expression of Egr-1 in late stage emphysema.
Expression of Egr-1 in late stage emphysema.
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DOI：
10.1016/s0002-9440(10)64646-9
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发表时间：
2000-10
期刊：
影响因子：
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通讯作者：
Weisu Zhang;S. Yan;Aiping Zhu;Y. Zou;Matthew R. Williams;G. Godman;B. Thomashow;M. Ginsburg;David M. Stern;S. Yan
中科院分区：
文献类型：
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作者：
Weisu Zhang;S. Yan;Aiping Zhu;Y. Zou;Matthew R. Williams;G. Godman;B. Thomashow;M. Ginsburg;David M. Stern;S. Yan
转录因子早期生长反应(Egr)-1是急性组织损伤后快速、短暂表达的一种即刻早期基因产物。相反，在本报告中，我们证明，与其他基因（包括转录因子Sp1）的广泛调查相比，在没有急性感染的临床或解剖学证据的情况下，接受肺减量手术的晚期肺气肿患者的肺组织显示出选择性和明显持续的Egr-1转录本和抗原的增加，其水平没有显着改变。Egr-1在支气管和血管壁平滑肌细胞、肺泡巨噬细胞和部分血管内皮中表达增强尤为明显。32p标记的Egr探针凝胶位移分析显示，肺气肿肺核提取物的条带与Egr-1抗体超移。Egr-1具有调控肺气肿病理生理相关基因的能力，即与细胞外基质形成和重塑、血栓形成相关的基因，以及编码细胞因子/趋化因子和生长因子的基因。因此，我们建议进一步分析Egr-1，它似乎在晚期肺气肿患者中持续上调，可能为了解这种破坏性肺部疾病的发病机制以及Egr-1生物学的新方面提供见解。
The transcription factor early growth response (Egr)-1 is an immediate-early gene product rapidly and transiently expressed after acute tissue injury. In contrast, in this report we demonstrate that lung tissue from patients undergoing lung reduction surgery for advanced emphysema, without clinical or anatomical evidence of acute infection, displays a selective and apparently sustained increase in Egr-1 transcripts and antigen, compared with a broad survey of other genes, including the transcription factor Sp1, whose levels were not significantly altered. Enhanced Egr-1 expression was especially evident in smooth muscle cells of bronchial and vascular walls, in alveolar macrophages, and some vascular endothelium. Gel shift analysis with32P-labeled Egr probe showed a band with nuclear extracts from emphysematous lung which was supershifted with antibody to Egr-1. Egr-1 has the capacity to regulate genes relevant to the pathophysiology of emphysema, namely those related to extracellular matrix formation and remodeling, thrombogenesis, and those encoding cytokines/chemokines and growth factors. Thus, we propose that further analysis of Egr-1, which appears to be up-regulated in a sustained fashion in patients with late stage emphysema, may provide insights into the pathogenesis of this destructive pulmonary disease, as well as a new facet in the biology of Egr-1.