F-M Wang1, D Song2, Y Pang2, Y Song3, F Yu4, M-H Zhao5. 1. Renal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, PR China Key Laboratory of Renal Disease, Ministry of Health of China, PR China; Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, PR China Institute of Nephrology, Zhongda Hospital, Southeast University, Nanjing, PR China. 2. Renal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, PR China Key Laboratory of Renal Disease, Ministry of Health of China, PR China; Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, PR China. 3. Department of Nephrology, the First Affiliated Hospital of Chinese PLA General Hospital, Beijing, PR China. 4. Renal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, PR China Key Laboratory of Renal Disease, Ministry of Health of China, PR China; Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, PR China Department of Nephrology, Peking University International Hospital, Beijing, PR China yufengevert1@sina.com songyan0209@163.com. 5. Renal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, PR China Key Laboratory of Renal Disease, Ministry of Health of China, PR China; Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, PR China Peking-Tsinghua Center for Life Sciences, Beijing, PR China.
Abstract
OBJECTIVE: Our previous study showed that plasma levels of factor H (FH) were significantly decreased in patients with lupus nephritis and reflected lupus nephritis activity. The aim of this study was to further investigate in vitro biofunctions of plasma FH in patients with lupus nephritis. METHODS: FH was purified from the first run of plasma exchange in four active lupus nephritis patients and two non-renal involvement systemic lupus erythematosus (SLE) patients, and plasma from two healthy controls. Then, the biofunctions of the purified FH were analyzed. In addition, FH exons sequencing analysis was performed. RESULTS: Homogeneous FH was purified from the plasma fractions and the purity of the purified FH was comparable to the commercial FH. The abilities of FH binding with C3b and mCRP, and its protecting abilities from the lysis of sheep erythrocytes, from No. 3 and No. 4 lupus nephritis patients, decreased significantly compared with those in normal controls. The purified FH from lupus nephritis patients Nos. 2-4 could not induce the phagocytosis of late apoptotic cells significantly compared with normal controls. All four lupus nephritis patients had the known SNP rs1061147 (SCR5, A307A), rs1061170 (SCR7, Y402H), CM050194 (SCR20, S1191W) and CM010322 (SCR20, V1197A), which might be associated with the above dysfunctions. CONCLUSIONS: Dysfunctions of FH, including the regulations of complement alternative pathway and the clearance of apoptotic cells, were found in some active lupus nephritis patients, which were associated with their clinical phenotypes. The FH SNPs might contribute to the dysfunctions of FH in patients with lupus nephritis.
OBJECTIVE: Our previous study showed that plasma levels of factor H (FH) were significantly decreased in patients with lupus nephritis and reflected lupus nephritis activity. The aim of this study was to further investigate in vitro biofunctions of plasma FH in patients with lupus nephritis. METHODS:FH was purified from the first run of plasma exchange in four active lupus nephritispatients and two non-renal involvement systemic lupus erythematosus (SLE) patients, and plasma from two healthy controls. Then, the biofunctions of the purified FH were analyzed. In addition, FH exons sequencing analysis was performed. RESULTS: Homogeneous FH was purified from the plasma fractions and the purity of the purified FH was comparable to the commercial FH. The abilities of FH binding with C3b and mCRP, and its protecting abilities from the lysis of sheep erythrocytes, from No. 3 and No. 4 lupus nephritispatients, decreased significantly compared with those in normal controls. The purified FH from lupus nephritispatients Nos. 2-4 could not induce the phagocytosis of late apoptotic cells significantly compared with normal controls. All four lupus nephritispatients had the known SNP rs1061147 (SCR5, A307A), rs1061170 (SCR7, Y402H), CM050194 (SCR20, S1191W) and CM010322 (SCR20, V1197A), which might be associated with the above dysfunctions. CONCLUSIONS:Dysfunctions of FH, including the regulations of complement alternative pathway and the clearance of apoptotic cells, were found in some active lupus nephritispatients, which were associated with their clinical phenotypes. The FH SNPs might contribute to the dysfunctions of FH in patients with lupus nephritis.
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