MurineCcl2/Cx3cr1Deficiency Results in Retinal Lesions Mimicking Human Age-Related Macular Degeneration
Author(s) -
Jingsheng Tuo,
Christine M. Bojanowski,
Min Zhou,
Defen Shen,
Robert J. Ross,
Kevin I. Rosenberg,
D. Joshua Cameron,
Chunyue Yin,
Jeffrey A. Kowalak,
Zhengping Zhuang,
Kang Zhang,
ChiChao Chan
Publication year - 2007
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.935
H-Index - 218
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.07-0051
Subject(s) - cx3cr1 , macular degeneration , biology , retina , retinal degeneration , retinal pigment epithelium , retinal , endoplasmic reticulum , drusen , lipofuscin , neurodegeneration , pathology , ccl2 , microbiology and biotechnology , chemokine , medicine , immunology , neuroscience , inflammation , ophthalmology , biochemistry , chemokine receptor , disease
Senescent Ccl2(-/-) mice are reported to develop cardinal features of human age-related macular degeneration (AMD). Loss-of-function single-nucleotide polymorphisms within CX3CR1 are also found to be associated with AMD. The authors generated Ccl2(-/-)/Cx3cr1(-/-) mice to establish a more characteristic and reproducible AMD model.
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