Jun Ji1, Qiong Xu2, Xia He2, Xiao-Ling Chen2, Jianan Yang3. 1. Department of Cardiovascular Surgery, University of Chinese Academy of Sciences Shenzhen Hospital, Shenzhen, China. 2. Department of Pathology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Hospital, Shenzhen, China. 3. Department of Cardiovascular Surgery, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Hospital, Shenzhen, China.
Abstract
OBJECTIVES: The aim of this study was to explore the differential expression profiles of microRNAs (miRNAs) in paraffin-embedded acute aortic dissection (AAD) tissues to find potential biomarkers for this disease. METHODS: A total of 92 paraffin-embedded tissue specimens were collected from 92 patients with AAD who underwent surgical replacement. Among these specimens, 54 had partial normal aortic segments (smooth intima surface, non-atherosclerotic lesions) in proximal crevasse of aorta. Samples of these segments were taken 1 cm away from aortic lesions as the control group, after eliminating the tunica adventitia tissues. miRNA expression profiles were obtained by miRNA microarray analysis. Differentially expressed miRNAs were found by comparing the AAD group with the control group and were verified by fluorescence real-time quantitative polymerase chain reaction and by fluorescence in situ hybridization. RESULTS: A total of 71 differentially expressed miRNAs were detected. Twenty-two were up-regulated and 49 were down-regulated. Four up-regulated miRNAs (hsa-miR-636, hsa-miR-142-3p, hsa-miR-425-3p, hsa-miR-191-3p) were selected for validation by real-time fluorescence quantitative polymerase chain reaction and fluorescence in situ hybridization. In the fluorescence real-time quantitative polymerase chain reaction analysis, only hsa-miR-636 showed a statistically significant difference in the AAD versus control comparison (3.3-fold, P = 0.012). The fluorescence in situ hybridization validation showed that the expression level of hsa-miR-636 was significantly increased in the AAD versus control comparison (P < 0.001), with average optical densities of 61.29 ± 16.83 in the AAD group and 9.30 ± 3.98 in the control group. CONCLUSIONS: Hsa-miR-636 is involved in the pathogenesis of AAD and may be a potential biomarker for this disease.
OBJECTIVES: The aim of this study was to explore the differential expression profiles of microRNAs (miRNAs) in paraffin-embedded acute aortic dissection (AAD) tissues to find potential biomarkers for this disease. METHODS: A total of 92 paraffin-embedded tissue specimens were collected from 92 patients with AAD who underwent surgical replacement. Among these specimens, 54 had partial normal aortic segments (smooth intima surface, non-atherosclerotic lesions) in proximal crevasse of aorta. Samples of these segments were taken 1 cm away from aortic lesions as the control group, after eliminating the tunica adventitia tissues. miRNA expression profiles were obtained by miRNA microarray analysis. Differentially expressed miRNAs were found by comparing the AAD group with the control group and were verified by fluorescence real-time quantitative polymerase chain reaction and by fluorescence in situ hybridization. RESULTS: A total of 71 differentially expressed miRNAs were detected. Twenty-two were up-regulated and 49 were down-regulated. Four up-regulated miRNAs (hsa-miR-636, hsa-miR-142-3p, hsa-miR-425-3p, hsa-miR-191-3p) were selected for validation by real-time fluorescence quantitative polymerase chain reaction and fluorescence in situ hybridization. In the fluorescence real-time quantitative polymerase chain reaction analysis, only hsa-miR-636 showed a statistically significant difference in the AAD versus control comparison (3.3-fold, P = 0.012). The fluorescence in situ hybridization validation showed that the expression level of hsa-miR-636 was significantly increased in the AAD versus control comparison (P < 0.001), with average optical densities of 61.29 ± 16.83 in the AAD group and 9.30 ± 3.98 in the control group. CONCLUSIONS:Hsa-miR-636 is involved in the pathogenesis of AAD and may be a potential biomarker for this disease.