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角膜蛋白聚糖促进角膜上皮伤口愈合。

Lumican promotes corneal epithelial wound healing.

作者信息

Liu Chia-Yang, Kao Winston Whei-Yang

机构信息

Department of Ophthalmology, College of Medicine, Edith J. Crawley Vision Research Center, University of Cincinnati, Cincinnati, OH, USA.

出版信息

Methods Mol Biol. 2012;836:285-90. doi: 10.1007/978-1-61779-498-8_18.

Abstract

Lumican regulates collagenous matrix assembly as a keratan sulfate proteoglycan in the cornea and is also present in the connective tissues of other organs and embryonic corneal stroma as a glycoprotein. In normal unwounded cornea, lumican is expressed by stromal keratocytes. Interestingly, injured mouse corneal epithelium ectopically and transiently expresses lumican during the early phase of wound healing, suggesting a potential lumican functionality unrelated to regulation of collagen fibrillogenesis, e.g., modulation of epithelial cell adhesion or migration. Healing of a corneal epithelial injury in lumican knockout (Lum(-/-)) mice was significantly delayed compared with Lum(+/-) mice. Addition of purified lumican to cultured medium promoted re-epithelialization and enhanced cell proliferation of wild-type mouse corneal epithelial cells in an organ culture. Therefore, administration of lumican may be beneficial for treating epithelial defects in the cornea and other tissues.

摘要

角膜中的核心蛋白聚糖作为一种硫酸角质素蛋白聚糖调节胶原基质组装,并且作为一种糖蛋白也存在于其他器官的结缔组织和胚胎角膜基质中。在正常未受伤的角膜中,核心蛋白聚糖由基质角膜细胞表达。有趣的是,受伤的小鼠角膜上皮在伤口愈合早期异位且短暂地表达核心蛋白聚糖,这表明核心蛋白聚糖具有与调节胶原纤维形成无关的潜在功能,例如调节上皮细胞黏附或迁移。与Lum(+/-)小鼠相比,核心蛋白聚糖基因敲除(Lum(-/-))小鼠的角膜上皮损伤愈合明显延迟。在器官培养中,向培养基中添加纯化的核心蛋白聚糖可促进野生型小鼠角膜上皮细胞的再上皮化并增强其细胞增殖。因此,给予核心蛋白聚糖可能有益于治疗角膜和其他组织中的上皮缺损。

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