Deficiency of the complement regulatory protein CD59 accelerates the development of diabetes-induced atherosclerosis in mice.

Abstract Aims Clinical and experimental evidence supports a strong link between the complement system, complement regulatory proteins and the pathogenesis of diabetes vascular complications. We previously reported that the complement regulatory protein CD59 is inactivated by glycation in humans with diabetes. Our objective for this study is to assess experimentally how the deficiency of CD59 impacts the development of diabetic atherosclerosis in vivo . Methods We crossed mCD59 sufficient and deficient mice into the ApoE −/− background to generate mCd59ab +/+ / ApoE −/− and mCd59ab −/− / ApoE −/− mice, and induced diabetes by multiple low dose injections of streptozotocin. Atherosclerosis was detected by hematoxylin and eosin (HE p p p p p mCD59ab +/+ /ApoE −/− ) counterpart. Conclusions The deficiency of CD59 accelerates the development of diabetic atherosclerosis.