Jiang-hua Wang1, Dong Jiang2, Hui-yng Rao2, Jing-min Zhao3, Yu Wang4, Lai Wei5. 1. Peking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, No. 11, Xizhimen South Street, Beijing 100044, China; Chinese Center for Disease Control and Prevention, 155 Changbai Road, Changping District, Beijing 102206, China. 2. Peking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, No. 11, Xizhimen South Street, Beijing 100044, China. 3. 302 Military Hospital of China, Beijing, China. 4. Chinese Center for Disease Control and Prevention, 155 Changbai Road, Changping District, Beijing 102206, China. Electronic address: wangyu@chinacdc.cn. 5. Peking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, No. 11, Xizhimen South Street, Beijing 100044, China; Chinese Center for Disease Control and Prevention, 155 Changbai Road, Changping District, Beijing 102206, China. Electronic address: weilai@pkuph.edu.cn.
Abstract
OBJECTIVES: MicroRNA-122 has been shown to be crucial for efficient HCV RNA replication in vitro. Pretreatment intrahepatic microRNA-122 levels in chronic hepatitis C (CHC) patients have been associated with the outcomes of interferon therapy. Here, we determined microRNA-122 serum levels in CHC patients and healthy donors using an absolute quantification approach and evaluated the correlation with liver inflammation grades and serum alanine aminotransferase (ALT) levels. METHODS: Serum samples were collected from 105 treatment-naive CHC patients, 11 acute hepatitis patients, and 33 healthy donors. Serum microRNA-122 was measured using the TaqMan RT-qPCR. The cycle threshold values were converted to copy numbers by drawing a standard curve using a chemical synthetic standard. For accurate quantification, copy numbers were further normalized according to the recovery ratios of spiked-in cel-miR-39. RESULTS: Serum levels of microRNA-122 were significantly higher in acute hepatitis and CHC patients than in healthy donors (p<0.001). However, there was no significant association between microRNA-122 and ALT serum levels or liver inflammation grades. CONCLUSIONS: The present study showed that serum microRNA-122 was elevated in acute and chronic hepatitis patients. However, this biomarker for acute liver injury did not reflect the liver inflammation activity in CHC patients.
OBJECTIVES: MicroRNA-122 has been shown to be crucial for efficient HCV RNA replication in vitro. Pretreatment intrahepatic microRNA-122 levels in chronic hepatitis C (CHC) patients have been associated with the outcomes of interferon therapy. Here, we determined microRNA-122 serum levels in CHCpatients and healthy donors using an absolute quantification approach and evaluated the correlation with liver inflammation grades and serum alanine aminotransferase (ALT) levels. METHODS: Serum samples were collected from 105 treatment-naive CHCpatients, 11 acute hepatitispatients, and 33 healthy donors. Serum microRNA-122 was measured using the TaqMan RT-qPCR. The cycle threshold values were converted to copy numbers by drawing a standard curve using a chemical synthetic standard. For accurate quantification, copy numbers were further normalized according to the recovery ratios of spiked-in cel-miR-39. RESULTS: Serum levels of microRNA-122 were significantly higher in acute hepatitis and CHCpatients than in healthy donors (p<0.001). However, there was no significant association between microRNA-122 and ALT serum levels or liver inflammation grades. CONCLUSIONS: The present study showed that serum microRNA-122 was elevated in acute and chronic hepatitispatients. However, this biomarker for acute liver injury did not reflect the liver inflammation activity in CHCpatients.
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