| Objective: To investigate the role of MBD2in ApoE-deficient mouse employed as amodel of age-related macular degeneration (AMD).Methods: Eight-week-old Mbd2-/-ApoE-/-mice (n=12,24eyes) and ApoE-/-mice(n=12,24eyes) were fed with Western-type diet for4months. Then the mice weresacrificed, total serum cholesterol levels were analyzed and Bruch’s membranes (BM)of the eyes were prepared for ultrastructural observation by transmission electronmicroscopy. Moreover, intercellular adhesion molecule-1(ICAM-1) immunoreactivitieswere evaluated by fluorescence microscope in sections of the eyes of both groups forfurther understanding the function mechanism of MBD2.Results: The levels of the total serum cholesterol in ApoE-/-mice showed no obviousdifference to that of Mbd2-/-ApoE-/-mice (P>0.05). Transmission electron microscopyshowed AMD-like lesions in ApoE-/-mice: various vacuoles accumulated in Bruch’smembrane, notable outer collagenous layer deposits and dilated basal infoldings ofRPE. More than that, ApoE-/-mice had a much thicker BM than Mbd2-/-ApoE-/-mice(p<0.05). As for the expression of ICAM-1in choroid exhibited by fluorescence micrographs, ApoE-/-mice is higher than Mbd2-/-ApoE-/-mice.Conclusions: Deficiency of Mbd2reduces the depositions accumulated in BM andattenuates the lesions in the development of AMD via reducing endothelial activationand suppressing inflammatory response in choroid. Our study helps to provide a newtherapeutic approach to the clinical treatment of AMD. |