Cargando…

CCR3 and Choroidal Neovascularization

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly in industrialized countries. The “wet” AMD, characterized by the development of choroidal neovacularization (CNV), could result in rapid and severe loss of central vision. The critical role of vascul...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Yiwen, Huang, Deqiang, Xia, Xin, Wang, Zhengying, Luo, Lingyu, Wen, Rong
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039674/
https://www.ncbi.nlm.nih.gov/pubmed/21358803
http://dx.doi.org/10.1371/journal.pone.0017106
_version_ 1782198222290157568
author Li, Yiwen
Huang, Deqiang
Xia, Xin
Wang, Zhengying
Luo, Lingyu
Wen, Rong
author_facet Li, Yiwen
Huang, Deqiang
Xia, Xin
Wang, Zhengying
Luo, Lingyu
Wen, Rong
author_sort Li, Yiwen
collection PubMed
description Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly in industrialized countries. The “wet” AMD, characterized by the development of choroidal neovacularization (CNV), could result in rapid and severe loss of central vision. The critical role of vascular endothelial growth factor A (VEGF-A) in CNV development has been established and VEGF-A neutralization has become the standard care for wet AMD. Recently, CCR3 was reported to play an important role in CNV development and that CCR3 targeting was reported to be superior to VEGF-A targeting in CNV suppression. We investigated the role of CCR3 in CNV development using the Matrigel induced CNV and found that in both rats and mice, CNV was well-developed in the control eyes as well as in eyes treated with CCR3 antagonist SB328437 or CCR3 neutralizing antibodies. No statistically significant difference in CNV areas was found between the control and SB328437 or CCR3-ab treated eyes. Immunostaining showed no specific expression of CCR3 in or near CNV. In contrast, both VEGF-A neutralizing antibodies and rapamycin significantly suppressed CNV. These results indicate that CCR3 plays no significant role in CNV development and question the therapeutic approach of CCR3 targeting to suppress CNV. On the other hand, our data support the therapeutic strategies of VEGF-A and mTOR (mammalian target of rapamycin) targeting for CNV.
format Text
id pubmed-3039674
institution National Center for Biotechnology Information
language English
publishDate 2011
publisher Public Library of Science
record_format MEDLINE/PubMed
spelling pubmed-30396742011-02-25 CCR3 and Choroidal Neovascularization Li, Yiwen Huang, Deqiang Xia, Xin Wang, Zhengying Luo, Lingyu Wen, Rong PLoS One Research Article Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly in industrialized countries. The “wet” AMD, characterized by the development of choroidal neovacularization (CNV), could result in rapid and severe loss of central vision. The critical role of vascular endothelial growth factor A (VEGF-A) in CNV development has been established and VEGF-A neutralization has become the standard care for wet AMD. Recently, CCR3 was reported to play an important role in CNV development and that CCR3 targeting was reported to be superior to VEGF-A targeting in CNV suppression. We investigated the role of CCR3 in CNV development using the Matrigel induced CNV and found that in both rats and mice, CNV was well-developed in the control eyes as well as in eyes treated with CCR3 antagonist SB328437 or CCR3 neutralizing antibodies. No statistically significant difference in CNV areas was found between the control and SB328437 or CCR3-ab treated eyes. Immunostaining showed no specific expression of CCR3 in or near CNV. In contrast, both VEGF-A neutralizing antibodies and rapamycin significantly suppressed CNV. These results indicate that CCR3 plays no significant role in CNV development and question the therapeutic approach of CCR3 targeting to suppress CNV. On the other hand, our data support the therapeutic strategies of VEGF-A and mTOR (mammalian target of rapamycin) targeting for CNV. Public Library of Science 2011-02-15 /pmc/articles/PMC3039674/ /pubmed/21358803 http://dx.doi.org/10.1371/journal.pone.0017106 Text en Li et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Li, Yiwen
Huang, Deqiang
Xia, Xin
Wang, Zhengying
Luo, Lingyu
Wen, Rong
CCR3 and Choroidal Neovascularization
title CCR3 and Choroidal Neovascularization
title_full CCR3 and Choroidal Neovascularization
title_fullStr CCR3 and Choroidal Neovascularization
title_full_unstemmed CCR3 and Choroidal Neovascularization
title_short CCR3 and Choroidal Neovascularization
title_sort ccr3 and choroidal neovascularization
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039674/
https://www.ncbi.nlm.nih.gov/pubmed/21358803
http://dx.doi.org/10.1371/journal.pone.0017106
work_keys_str_mv AT liyiwen ccr3andchoroidalneovascularization
AT huangdeqiang ccr3andchoroidalneovascularization
AT xiaxin ccr3andchoroidalneovascularization
AT wangzhengying ccr3andchoroidalneovascularization
AT luolingyu ccr3andchoroidalneovascularization
AT wenrong ccr3andchoroidalneovascularization