Mutation of human CD59 accelerates occurrence of human diabetic vascular proliferative complications

ZHANG Li; GAO Meihua

Abstract：Objective To confirm gene mutation of human complement regulatory protein CD59 accelerates occurrence of the vascular proliferative complication of human diabetes.Methods The recombinant pALTER-MAX plasmids containing respective human gene mutant CD59 cDNA and pcDNA were co-transfected into CHO cell by cation lipoid mediating method.Highly expressing cells were selected by flow cytometry,immunofluorescence technique,and immunohistochemistry technique.These cells were cultivated in high glucose,and the functions of restricting complement membrane attack complex formation of glycated HMCD59 and HNCD59 were detected by BCECF release test.ELISA was used to detect senlm levels of PDGF and bFGF in 30 diabetes patients without vascular proliferate complications and 30 type Ⅱ diabetes patients with vascular proliferate complications.Results Expressing rates of HMCD59 cells were 53.0%and 54.5%.while expressing rates of HNCD59 were 59.8%.BCECF releasing test indicted the releasing rate of glycated HMCD59 cells were significant higher than that of unglycated ones,while no significant difference of releasing rate was found between glycated HNCD59 cells and unglycated ones.The serum levels of PDGF and bFGF in diabetes patient with vascular proliferate complications were obviously increased as compared with that of diabetes patient without vascular proliferate complications(P＜0.01).Conclusion The decrease of the autologous complementary constriction of glycated human mutant CD59 possibly resuhs in or accelerates the development of human diabetic vascular proliferative complications.