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糖尿病大鼠皮肤伤口愈合再上皮化过程中水通道蛋白 3 表达受损。

Impaired aquaporin 3 expression in reepithelialization of cutaneous wound healing in the diabetic rat.

机构信息

Department of Gerontological Nursing/Wound Care Management, Division of Health Science and Nursing, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

出版信息

Biol Res Nurs. 2013 Jul;15(3):347-55. doi: 10.1177/1099800412437032. Epub 2012 Apr 23.

DOI:10.1177/1099800412437032
PMID:22531364
Abstract

Impaired cutaneous wound healing is a serious complication of diabetes mellitus (DM). Currently, little is known about reepithelialization in DM. However, recent studies identified aquaporin 3 (AQP3), a transmembrane protein that functions as a pore-like passive transporter, to be a key molecule in cutaneous epidermal wound healing. AQP3 expression is downregulated in response to tumor necrosis factor-alpha (TNF- α). Given that systemic TNF-α levels are functionally connected to impaired healing in diabetic mice and that both diabetic and Aqp3-deficient animals exhibit impaired reepithelialization, the authors hypothesized that impaired AQP3 expression might contribute to diabetes-impaired wound healing. In the present study, the authors examined AQP3 expression in the regenerating epidermis during cutaneous full thickness wound healing and in intact skin of a streptozotocin-induced diabetic rat model. Aqp3 messenger RNA expression levels were decreased in wounds of DM rats compared to controls. Immunohistochemical analysis showed an absence of AQP3 in the stratum spinosum of the regenerating epidermis in the DM group, whereas the stratum basale was positive for AQP3 in both groups. In summary, these findings suggest that there may be a relationship between impaired AQP3 expression and diabetes-delayed reepithelialization. Thus, future nursing studies should focus on this mechanism in diabetic wound healing.

摘要

糖尿病(DM)患者的皮肤创伤愈合受损是一种严重的并发症。目前,人们对 DM 患者的上皮再形成过程知之甚少。然而,最近的研究发现水通道蛋白 3(AQP3)是一种跨膜蛋白,作为一种类似孔的被动转运蛋白,是皮肤表皮创伤愈合的关键分子。AQP3 的表达受到肿瘤坏死因子-α(TNF-α)的下调。鉴于系统 TNF-α 水平与糖尿病小鼠的愈合受损功能相关,并且糖尿病和 Aqp3 缺陷动物均表现出上皮再形成受损,作者假设 AQP3 表达受损可能导致糖尿病伤口愈合受损。在本研究中,作者检查了皮肤全层创伤愈合过程中再生表皮和链脲佐菌素诱导的糖尿病大鼠模型完整皮肤中的 AQP3 表达。与对照组相比,DM 大鼠伤口中的 Aqp3 信使 RNA 表达水平降低。免疫组织化学分析显示,DM 组再生表皮的棘层中缺乏 AQP3,而两组的基底层均为 AQP3 阳性。总之,这些发现表明 AQP3 表达受损与糖尿病上皮再形成延迟之间可能存在关系。因此,未来的护理研究应集中在糖尿病伤口愈合的这一机制上。

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