Smith R S, John S W, Zabeleta A, Davisson M T, Hawes N L, Chang B
The Jackson Laboratory, Bar Harbor, ME 04609, USA.
Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2191-5. doi: 10.1073/pnas.040531597.
Ocular neovascularization is the leading cause of blindness in developed countries and often causes rapid loss of vision in age-related macular degeneration. Acute visual loss is most often due to hemorrhage from new vessels that have extended from the choroid into the subretinal space. Growth of abnormal vessels beneath the retina in this condition is known as subretinal neovascularization (SRN). Age-related animal models of macular degeneration and SRN have not been described. Current animal models of SRN depend on chemical or physical stimuli to initiate growth of subretinal vessels. The genes responsible for age-related human macular degeneration with SRN have not been firmly identified. We report an angiogenic phenotype in Bst/+ mice that is age-related, clinically evident, and resembles human SRN. This represents a spontaneous, genetically determined model of SRN. Bst/+ mice offer the possibility of exploring the molecular mechanisms of SRN without the need for exogenous agents.
眼部新生血管形成是发达国家失明的主要原因,并且在年龄相关性黄斑变性中常常导致视力迅速丧失。急性视力丧失最常见的原因是从脉络膜延伸至视网膜下间隙的新生血管出血。在这种情况下,视网膜下异常血管的生长被称为视网膜下新生血管形成(SRN)。尚未描述年龄相关性黄斑变性和SRN的动物模型。目前的SRN动物模型依赖化学或物理刺激来启动视网膜下血管的生长。导致伴有SRN的年龄相关性人类黄斑变性的基因尚未得到确切鉴定。我们报告了Bst/+小鼠中一种与年龄相关、临床上明显且类似于人类SRN的血管生成表型。这代表了一种自发的、由基因决定的SRN模型。Bst/+小鼠提供了无需外源性试剂即可探索SRN分子机制的可能性。