Aim: To investigate the function of human mutant CD59 in diabetic pathology.
Methods: The recombinant PALTER-MAX plasmid containing human mutant CD59 cDNA and pcDNA plasmid were cotransfected into CHO cells using cation lipoid mediating method. Highly expressed cells were selected by flow cytometry and Western blot, which were then cultivated in high glucose. 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 the serum concentration of PDGF-BB and VEGF in 30 patients of typeII diabetes without vascular proliferate complication and 30 typeII diabetes patients with vascular proliferate complication.
Results: The expression rate of HM1CD59, HM2CD59, HNCD59 cells was 53.7%, 54.5% and 59.8%, respectively. BCECF release test indicated the release rate of glycated HMCD59 cells was higher than that of unglycated ones (P<0.01)while no significant differences were found between normal HNCD59 cells and glycated ones. The serum concentration of PDGF-BB and VEGF in patients with typeII diabetes markedly increased (P<0.01).
Conclusion: The decrease of glycated restricting complement membrane attack complex results in the accelerating of human vascular proliferate complication of diabetes.