This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.The hypothesis under evaluation in this project is that in human diabetes, glycation-inactivation of CD59 leads first to increased MAC deposition in diabetic tissues and then to increased MAC-induced release of growth factors and pro-inflammatory and pro-thrombotic cytokines that stimulate proliferation, inflammation and thrombosis as well as expansion of the extracellular matrix and thereby, synergistically with other hyperglycemia-induced pathways, promotes the development of micro- and macrovascular proliferative disease and glomerulosclerosis. Specifically, we will evaluate whether glycation of CD59 is altered with changing glycemia in human subjects with type 1 or type 2 diabetes. This portion of the study will be performed in about 50 persons.
A second aim will be to determine whether glycated CD59 is elevated in persons with impaired glucose tolerance without overt diabetes. This portion of the study will be conducted in up to 100 persons This is a single site study to address a population based physiologic question.
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