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Updated: May 28, 2026

Murine Full-thickness Skin Transplantation
Published on: January 2, 2017
Chronic graft dysfunction and improvement by cytokine response modifier a protein transfection
Zheng Xiao1, Juan Shan, Chengwen Li
1Key Laboratory of Transplant Engineering and Immunology of Ministry Health of China, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, PR China.
Objectives:
Cytokine response modifier A protein is a caspase inhibitor that inhibits caspase activity and protects cells from apoptosis. Chronic cyclosporine nephropathy is a significant cause of chronic graft dysfunction. We explored cytokine response modifier A protein-alleviated chronic cyclosporine nephropathy for ways of improving chronic graft dysfunction.
Materials And Methods:
Cytokine response modifier A protein-transferring HK-2 cells were cultured with different concentrations of cyclosporine. Cytokine response modifier A protein mRNA and proteins were detected by real-time polymerase chain reaction and Western blot, cell viability was detected by (3-(4,5-Dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide), and apoptosis was detected by flow cytometry.
Results:
Cyclosporine caused a concentration-dependent and time-dependent loss of cell viability in HK-2 cells. Cytokine response modifier A protein mRNA was expressed at 48 and 72 hours (P < .05), while protein was detected at 72 hours. Cell viability in the cytokine response modifier A protein-transfected group was significantly greater than that of the control group when treated with 1 µg/mL, 10 µg/mL, or 20 µg/mL cyclosporine at 24 or 48 hours (P < .05). The apoptosis in cytokine response modifier A protein-transfected cells was significantly lower than that of controls (P < .05).
Conclusions:
Cytokine response modifier A protein protects renal cells from cyclosporine injury by inhibiting activated caspases. Cytokine response modifier A protein transfection may improve chronic cyclosporine nephropathy and provide for improving chronic graft dysfunction.
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