TFPI-VLDLR Pathway in Retinal Angiogenesis
Age-related macular degeneration (AMD) is the most common cause of severe and irreversible vision loss in older adults in the US. The key lesion in the eye is abnormal vessel growth in the retina. Although several risk factors have been named, what molecule triggers the abnormal vessel growth is still not clear. A recent study reported that similar abnormal vessel growth was found in the eyes of a mutant mouse which lacks very low density lipid receptor (vldlr). The current proposal is to examine the role of vldlr as well as its known up- and down-stream molecules on the abnormal vessel growth in the eye. We will use this mutant mouse model and look for potential differences between the normal control and the mutant mice. We will also use retinal vascular cell culture to determine if vldlr and related molecules are the key pathway to stimulate abnormal vessel growth. Identify key molecules responsible for abnormal vessel growth will provide us new targets to develop better treatment strategy for AMD.
Jiang A, Hu W, Meng H, Gao H, and Qiao X, (2009) Loss of VLDL receptor activates retinal endothelial cells and promotes angiogenesis, Invest Ophthalmol Vis Sci, 50:844-850.
Meng H, Hu W, Liang J, Jiang A, Wang W, Chang B, Gao H, and Qiao X, Early activation of multiple inflammatory cytokines and macrophage in vldlr deficient mice, in submission.
First published on: June 10, 2008
Last modified on: June 11, 2008