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Differential expression of cyclooxygenases in hypertrophic scar and keloid tissues.

机译:环氧酶的微分表达式肥厚性瘢痕和瘢痕疙瘩组织。

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摘要

Hypertrophic scar (HS) and keloid (KL) are two forms of an abnormal cutaneous scarring process, mainly characterized by excessive extracellular matrix deposition and fibroblast proliferation. Despite the increased understanding of the molecular and cellular events leading to HS and KL, the pathogenesis of these lesions remains poorly understood. A pivotal role in the formation of abnormal scars has been ascribed to transforming growth factor-beta, whose activity appears to be mediated through a link with pathways acting via cyclooxygenases (COX-1 and COX-2). To date, there is no report on the in vivo expression of COX-1 and COX-2 in human HS and KL tissues. Therefore, using immunohistochemistry and Western blot analysis, we investigated 36 cases of KL, 32 cases of HS, and 25 cases of normal skin in order to define the localization and distribution of COX-1 and COX-2 in the tissues of these scar lesions and the overlying epidermis. The results mainly show the following: (a) a significant overexpression of COX-1 in HS tissues and the overlying epidermis as compared with normal skin and KL tissues and (b) a significant overexpression of COX-2 in KL tissue and the overlying epidermis in contrast to normal skin and HS tissues. Our data support the hypothesis that both COXs are involved in the pathogenesis of scar lesions in different ways and, particularly, COX-1 in the formation of HS and COX-2 in the formation of KL. In addition, the overexpression of COX-1 and COX-2 in the epidermis overlying HS and KL tissues, respectively, underlines the importance of epithelial-mesenchymal interactions in the pathogenesis of scar lesions.
机译:肥厚性疤痕(HS)和瘢痕疙瘩(吉隆坡)是两个形式的异常皮肤疤痕的过程,主要表现为过度的细胞外基质沉积和成纤维细胞增殖。尽管增加的理解分子和细胞导致商品和事件吉隆坡,这些病变的发病机制仍然存在知之甚少。归因于异常疤痕形成转化生长因子,其活动似乎是通过与介导通路通过环氧酶(COX-1和行动cox - 2)。在人类HS vivo COX-1和cox - 2的表达和KL组织。免疫组织化学和免疫印迹分析,我们调查了36例KL, 32例HS,和25例正常皮肤来定义COX-1的定位和分布cox - 2在这些疤痕的组织损伤上覆表皮。以下几点:(a)一个重要的过度COX-1的商品组织和覆盖表皮与正常皮肤和吉隆坡组织和(b)的一个重要过度cox - 2在KL组织和表皮覆盖与正常皮肤和海关组织。考克斯都支持假设参与疤痕病变的发病机理不同的方法,特别是COX-1形成HS和cox - 2在KL的形成。此外,COX-1和超表达cox - 2在表皮上覆HS和吉隆坡组织,分别强调了重要性epithelial-mesenchymal交互的疤痕病变的发病机理。

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