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糖尿病角膜伤口愈合的异常机制。

Deviated mechanism of wound healing in diabetic corneas.

作者信息

Chikama Tai-ichiro, Wakuta Makiko, Liu Yang, Nishida Teruo

机构信息

Department of Ophthalmology, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube City, Yamaguchi 755-8505, Japan.

出版信息

Cornea. 2007 Oct;26(9 Suppl 1):S75-81. doi: 10.1097/ICO.0b013e31812f6d8e.

Abstract

We examined phenotypic changes during the wound healing process in the corneal epithelium of Goto-Kakizaki (GK) rats, a spontaneous model of type 2 diabetes mellitus. In this article, we provide an overview of our and other groups' research and describe the clinical features of diabetic keratopathy. We observed that the rate of corneal epithelial wound closure was decreased in GK rats compared with Wistar rats. Immunoreactivity for Cx43, K14, and Ki-67 was detected in the 2 layers of cells adjacent to the basement membrane in the corneal epithelium of GK rats, whereas only the single basal layer of cells was positive for these proteins in the corneal epithelium of Wistar rats. The frequency of Ki-67-positive cells was greater in GK rats than in Wistar rats in the intact corneal epithelium and during wound healing. The GK rat represents delayed corneal epithelial wound closure as well as that which is observed in human diabetic keratopathy. Furthermore, these results indicate a possibility of functional deviation in corneal epithelial cells with diabetes mellitus.

摘要

我们研究了2型糖尿病自发模型——Goto-Kakizaki(GK)大鼠角膜上皮伤口愈合过程中的表型变化。在本文中,我们概述了我们和其他团队的研究,并描述了糖尿病角膜病变的临床特征。我们观察到,与Wistar大鼠相比,GK大鼠角膜上皮伤口闭合速率降低。在GK大鼠角膜上皮中,与基底膜相邻的两层细胞检测到Cx43、K14和Ki-67的免疫反应性,而在Wistar大鼠角膜上皮中,只有单一的基底层细胞对这些蛋白呈阳性。在完整角膜上皮和伤口愈合过程中,GK大鼠中Ki-67阳性细胞的频率高于Wistar大鼠。GK大鼠表现出角膜上皮伤口闭合延迟,这与人类糖尿病角膜病变中观察到的情况相同。此外,这些结果表明糖尿病患者角膜上皮细胞可能存在功能偏差。

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