New Protein Target Key to Prevent Macular DegenerationLast Updated: June 17, 2009. Blocking the activity of the protein eosinophil/mast cell chemokine receptor can reduce the abnormal blood vessel growth that leads to age-related macular degeneration, a leading cause of blindness worldwide, according to a study published online June 14 in Nature.
WEDNESDAY, June 17 (HealthDay News) -- Blocking the activity of the protein eosinophil/mast cell chemokine receptor (CCR3) can reduce the abnormal blood vessel growth that leads to age-related macular degeneration (AMD), a leading cause of blindness worldwide, according to a study published online June 14 in Nature.
Atsunobu Takeda, of the University of Kentucky in Lexington, and colleagues examined eye tissue from people with and without AMD and observed the presence of CCR3 in the diseased eyes. The investigators used laser photocoagulation on the eyes of mice to induce choroidal neovascularization (CNV), the same disease mechanism that leads to blood vessel growth and blindness in AMD. The investigators then injected neutralizing antibodies against mouse CCR3 into the vitreous humor of the mouse eyes.
The investigators found that targeting the CCR3 protein inhibited development of CNV in mice by direct inhibition of endothelial cell proliferation, and was more effective (68 versus 57 percent) than targeting vascular endothelial growth factor A (VEGF-A), which is the current treatment for AMD. Also, the anti-CCR3 antibodies were not toxic to the retina as the VEGF-A targeting pharmacotherapy can be.
"Our findings suggest that CCR3 targeting may be a safe and viable strategy for early detection (using biocompatible quantum dots or other bioimaging fluorochromes, such as near infrared dyes) and treatment of CNV (by receptor or ligand targeting), and might be superior to the current standard of care," the authors write.
|Previous: Wealth and Ethnicity Affect Well Woman Screening Rates||Next: Rivaroxaban Has Mixed Results in Acute Coronary Syndrome|
Reader comments on this article are listed below. Review our comments policy.