What is the role of CCR3 in choroidal neovascularization?

Yiwen Li; Deqiang Huang; Xin Xia; Zhengying Wang; Lingyu Luo; Rong Wen

doi:10.1007/978-1-4614-0631-0_36

What is the role of CCR3 in choroidal neovascularization?

Yiwen Li, Deqiang Huang, Xin Xia, Zhengying Wang, Lingyu Luo, Rong Wen

Ophthalmology

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Abstract

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) in CNV development has been clearly demonstrated and clinically VEGF neutralization has become standard care for wet AMD. Recently, CCR3 was reported to play an important role in CNV development and CCR3 targeting was believed to be superior to VEGF targeting for CNV suppression. Our data in the present work show that blocking CCR3 by a small molecule CCR3 antagonist SB 328437 or CCR3-neutralizing antibodies does not inhibit CNV in the Matrigel CNV models of rat and mouse, whereas VEGF-neutralizing antibodies or rapamycin effectively suppresses CNV. These results question the role of CCR3 in CNV development and the therapeutic approach to suppress CNV by CCR3 targeting.

Original language	English (US)
Title of host publication	Retinal Degenerative Diseases
Editors	Matthew LaVail, Robert Anderson, Christian Grimm, John Ash, Joe Hollyfield
Pages	279-284
Number of pages	6
DOIs	https://doi.org/10.1007/978-1-4614-0631-0_36
State	Published - 2012

Publication series

Name	Advances in Experimental Medicine and Biology
Volume	723
ISSN (Print)	0065-2598

Keywords

AMD
Angiogenesis
CCR3
CNV
Matrigel
Rapamycin
SB328437
VEGF-A

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)
Medicine(all)

Access to Document

10.1007/978-1-4614-0631-0_36

Cite this

What is the role of CCR3 in choroidal neovascularization? / Li, Yiwen; Huang, Deqiang; Xia, Xin; Wang, Zhengying; Luo, Lingyu; Wen, Rong.

Retinal Degenerative Diseases. ed. / Matthew LaVail; Robert Anderson; Christian Grimm; John Ash; Joe Hollyfield. 2012. p. 279-284 (Advances in Experimental Medicine and Biology; Vol. 723).

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

@inproceedings{eb3b8376f5b8470fbb24fb21ba351b5d,

title = "What is the role of CCR3 in choroidal neovascularization?",

abstract = "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) in CNV development has been clearly demonstrated and clinically VEGF neutralization has become standard care for wet AMD. Recently, CCR3 was reported to play an important role in CNV development and CCR3 targeting was believed to be superior to VEGF targeting for CNV suppression. Our data in the present work show that blocking CCR3 by a small molecule CCR3 antagonist SB 328437 or CCR3-neutralizing antibodies does not inhibit CNV in the Matrigel CNV models of rat and mouse, whereas VEGF-neutralizing antibodies or rapamycin effectively suppresses CNV. These results question the role of CCR3 in CNV development and the therapeutic approach to suppress CNV by CCR3 targeting.",

keywords = "AMD, Angiogenesis, CCR3, CNV, Matrigel, Rapamycin, SB328437, VEGF-A",

author = "Yiwen Li and Deqiang Huang and Xin Xia and Zhengying Wang and Lingyu Luo and Rong Wen",

note = "Funding Information: This work was supported by grants from the James and Esther King Biomedical Research Program of the State of Florida (YL), National Institutes of Health (R01EY015289 to RW, R01EY018586 to RW), Hope for Vision (RW), and the Department of Defense (W81XWH-09-1-0674 to RW). It was also supported by NIH core grant P30EY14801 and an unrestricted grant from Research to Prevent Blindness Inc. to Bascom Palmer Eye Institute.",

year = "2012",

doi = "10.1007/978-1-4614-0631-0_36",

language = "English (US)",

isbn = "9781461406303",

series = "Advances in Experimental Medicine and Biology",

pages = "279--284",

editor = "Matthew LaVail and Robert Anderson and Christian Grimm and John Ash and Joe Hollyfield",