Planck S R, Andresevic J, Chen J C, Holmes D L, Rodden W, Westra I, Wu S C, Huang X N, Kay G, Wilson D J
Department of Ophthalmology, Casey Eye Institute, Oregon Health Sciences University, Portland 97201-4197.
Curr Eye Res. 1992 Nov;11(11):1031-9. doi: 10.3109/02713689209015074.
Proliferative vitreoretinopathy (PVR) involves the formation of intravitreal fibrocellular membranes which may lead to traction retinal detachment and blindness. The cellular component of epiretinal membranes originates from the proliferation and migration of cells within the eye. Several growth factors and other cytokines are plausible candidates for directing the processes leading to membrane formation. A reproducible animal model is needed for experimental studies of cytokine expression during PVR induction or treatment. We found that intravitreal injection of > 10(6) mixed mononuclear leukocytes or adherent monocytes along with a trans-scleral incision through the pars plana leads to the development of PVR-like disease in rabbit eyes. The severity of the disease was related to the number of monocytes injected. Typically, organized membranes extending from the incision toward the optic nerve formed within one week. Progression to extensive traction retinal detachment required 1 to 4 weeks. Injection of up to 5 x 10(6) lymphocytes or freeze-thaw killed monocytes was ineffective, and coinjecting 100 micrograms endotoxin with the monocytes did not result in enhanced disease. The histological appearance of the epiretinal membranes was similar to human PVR membranes. Macrophage, cytokeratin-positive (epithelial), and fibroblast-like cells were present. Northern blot analysis of RNA extracted from the rabbit membranes revealed the presence of mRNA for acidic fibroblast growth factor (aFGF). Acidic FGF mRNA was not expressed by the injected monocytes. A comparable level of aFGF mRNA and also mRNAs for basic FGF, platelet-derived growth factor-B, and transforming growth factor beta were found in epiretinal membranes induced by a scleral incision in association with cryopexy.(ABSTRACT TRUNCATED AT 250 WORDS)
增殖性玻璃体视网膜病变(PVR)涉及玻璃体内纤维细胞性膜的形成,这可能导致牵拉性视网膜脱离和失明。视网膜前膜的细胞成分源自眼内细胞的增殖和迁移。几种生长因子和其他细胞因子可能是指导导致膜形成过程的候选因素。在PVR诱导或治疗过程中,需要一种可重复的动物模型来进行细胞因子表达的实验研究。我们发现,玻璃体内注射超过10⁶个混合单核白细胞或贴壁单核细胞,并通过睫状体扁平部进行经巩膜切口,可导致兔眼发生类似PVR的疾病。疾病的严重程度与注射的单核细胞数量有关。通常,在一周内会形成从切口向视神经延伸的有条理的膜。进展为广泛的牵拉性视网膜脱离需要1至4周。注射多达5×10⁶个淋巴细胞或冻融杀死的单核细胞无效,并且将100微克内毒素与单核细胞共同注射也不会导致疾病加重。视网膜前膜的组织学外观与人类PVR膜相似。存在巨噬细胞、细胞角蛋白阳性(上皮)和成纤维细胞样细胞。从兔膜中提取的RNA的Northern印迹分析显示存在酸性成纤维细胞生长因子(aFGF)的mRNA。注射的单核细胞不表达酸性FGF mRNA。在巩膜切口联合冷冻疗法诱导的视网膜前膜中发现了与碱性FGF、血小板衍生生长因子-B和转化生长因子β相当水平的aFGF mRNA以及它们的mRNA。(摘要截短于250字)