小鼠角膜新生血管化的碱烧伤损伤模型。
An alkali-burn injury model of corneal neovascularization in the mouse.
作者信息
Anderson Chastain, Zhou Qinbo, Wang Shusheng
机构信息
Department of Cell and Molecular Biology, Tulane University; Department of Ophthalmology, Tulane University;
出版信息
J Vis Exp. 2014 Apr 7(86):51159. doi: 10.3791/51159.
Under normal conditions, the cornea is avascular, and this transparency is essential for maintaining good visual acuity. Neovascularization (NV) of the cornea, which can be caused by trauma, keratoplasty or infectious disease, breaks down the so called 'angiogenic privilege' of the cornea and forms the basis of multiple visual pathologies that may even lead to blindness. Although there are several treatment options available, the fundamental medical need presented by corneal neovascular pathologies remains unmet. In order to develop safe, effective, and targeted therapies, a reliable model of corneal NV and pharmacological intervention is required. Here, we describe an alkali-burn injury corneal neovascularization model in the mouse. This protocol provides a method for the application of a controlled alkali-burn injury to the cornea, administration of a pharmacological compound of interest, and visualization of the result. This method could prove instrumental for studying the mechanisms and opportunities for intervention in corneal NV and other neovascular disorders.
在正常情况下，角膜是无血管的，这种透明度对于维持良好的视力至关重要。角膜新生血管形成（NV）可由外伤、角膜移植术或传染病引起，它打破了角膜所谓的“血管生成特权”，并形成多种甚至可能导致失明的视觉病理的基础。尽管有几种治疗选择，但角膜新生血管病变所带来的基本医疗需求仍未得到满足。为了开发安全、有效且有针对性的疗法，需要一个可靠的角膜NV模型和药物干预模型。在此，我们描述一种小鼠碱烧伤诱导的角膜新生血管化模型。本方案提供了一种对角膜施加可控碱烧伤、给予感兴趣的药理化合物并观察结果的方法。该方法可能对研究角膜NV及其他新生血管疾病的干预机制和机会具有重要作用。
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