Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3

10.1038/srep15702

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Main Authors: Tan, X, Fujiu, K, Manabe, I, Nishida, J, Yamagishi, R, Nagai, R, Yanagi, Y
Other Authors: DUKE-NUS MEDICAL SCHOOL
Format: Article
Published: Nature Publishing Group 2020
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Online Access:https://scholarbank.nus.edu.sg/handle/10635/180420
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spelling sg-nus-scholar.10635-1804202023-11-01T08:13:47Z Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3 Tan, X Fujiu, K Manabe, I Nishida, J Yamagishi, R Nagai, R Yanagi, Y DUKE-NUS MEDICAL SCHOOL complement component C3 animal C57BL mouse disease model granulocyte inflammation macrophage macular degeneration male metabolism monocyte mouse pathology retinal pigment epithelium subretinal neovascularization Animals Choroidal Neovascularization Complement C3 Disease Models, Animal Granulocytes Inflammation Macrophages Macular Degeneration Male Mice Mice, Inbred C57BL Monocytes Retinal Pigment Epithelium 10.1038/srep15702 Scientific Reports 5 15702 2020-10-26T08:54:20Z 2020-10-26T08:54:20Z 2015 Article Tan, X, Fujiu, K, Manabe, I, Nishida, J, Yamagishi, R, Nagai, R, Yanagi, Y (2015). Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3. Scientific Reports 5 : 15702. ScholarBank@NUS Repository. https://doi.org/10.1038/srep15702 2045-2322 https://scholarbank.nus.edu.sg/handle/10635/180420 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Nature Publishing Group Unpaywall 20201031
institution National University of Singapore
building NUS Library
continent Asia
country Singapore
Singapore
content_provider NUS Library
collection ScholarBank@NUS
topic complement component C3
animal
C57BL mouse
disease model
granulocyte
inflammation
macrophage
macular degeneration
male
metabolism
monocyte
mouse
pathology
retinal pigment epithelium
subretinal neovascularization
Animals
Choroidal Neovascularization
Complement C3
Disease Models, Animal
Granulocytes
Inflammation
Macrophages
Macular Degeneration
Male
Mice
Mice, Inbred C57BL
Monocytes
Retinal Pigment Epithelium
spellingShingle complement component C3
animal
C57BL mouse
disease model
granulocyte
inflammation
macrophage
macular degeneration
male
metabolism
monocyte
mouse
pathology
retinal pigment epithelium
subretinal neovascularization
Animals
Choroidal Neovascularization
Complement C3
Disease Models, Animal
Granulocytes
Inflammation
Macrophages
Macular Degeneration
Male
Mice
Mice, Inbred C57BL
Monocytes
Retinal Pigment Epithelium
Tan, X
Fujiu, K
Manabe, I
Nishida, J
Yamagishi, R
Nagai, R
Yanagi, Y
Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3
description 10.1038/srep15702
author2 DUKE-NUS MEDICAL SCHOOL
author_facet DUKE-NUS MEDICAL SCHOOL
Tan, X
Fujiu, K
Manabe, I
Nishida, J
Yamagishi, R
Nagai, R
Yanagi, Y
format Article
author Tan, X
Fujiu, K
Manabe, I
Nishida, J
Yamagishi, R
Nagai, R
Yanagi, Y
author_sort Tan, X
title Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3
title_short Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3
title_full Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3
title_fullStr Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3
title_full_unstemmed Choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component C3
title_sort choroidal neovascularization is inhibited via an intraocular decrease of inflammatory cells in mice lacking complement component c3
publisher Nature Publishing Group
publishDate 2020
url https://scholarbank.nus.edu.sg/handle/10635/180420
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