Expression of miRNA-155 in carotid atherosclerotic plaques of apolipoprotein E knockout (ApoE?/?) mice and the interventional effect of rapamycin |
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| Institution: | 1. Department of Neurology, The Affiliated Hospital of the Qingdao University, Qingdao, Shandong Province 266003, PR China;2. Central Laboratory, The Affiliated Hospital of the Qingdao University, Qingdao, Shandong Province 266003, PR China;3. Laboratory of Human Micromorphology, The Medical College of Qingdao University, Qingdao 266003, PR China;1. Key Laboratory of Bioactive Peptides of Yunnan Province/Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming 650223, Yunnan, China;2. University of Chinese Academy of Sciences, Beijing 100009, China;3. Life Sciences College of Nanjing Agricultural University, Nanjing 210095, Jiangsu, China;4. Sino-African Joint Research Center, Chinese Academy of Science, Wuhan, Hubei 430074, China;5. Intensive Care Unit, Subei People''s Hospital of Jiangsu Province, Yangzhou, Jiangsu 225001, China;1. Division of Molecular Regulation, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan;2. Department of Disaster Psychiatry, International Research Institute for Disaster Science, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan;3. Laboratory of Pharmacology, Faculty of Pharmaceutical Science, Aomori University, 2-3-1 Koubata, Aomori 030-0943, Japan;4. Department of Oral Anatomy and Developmental Biology, School of Dentistry, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan;5. Clinical Research Center for Diabetes, Tokushima University Hospital, 2-50-1 Kuramoto-cho, Tokushima 770-8503, Japan;6. Division of Microbiology and Immunology, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan;7. Department of Pediatric Dentistry, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama 230-8501, Japan;8. Department of Microbiology and Immunology, Aichi Medical University, Nagakute, Aichi 48-1955, Japan;1. Department of Oncology, Chinese PLA General Hospital, Beijing, China;2. Department of Gastroenterology, Chinese PLA General Hospital, Beijing, China;1. Liver Transplantation Center, First Affiliated Hospital, Nanjing Medical University, No. 300 Guangzhou Road, Nanjing 210029, China;2. Department of Radiotherapy, First Affiliated Hospital, Nanjing Medical University, No. 300 Guangzhou Road, Nanjing 210029, China;1. Department of Oncology, Taipei Veterans General Hospital, Taipei, Taiwan;2. Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan;3. Department of Pharmacy, Taipei Veterans General Hospital, Taipei, Taiwan;4. Institute of Environmental and Occupational Health Sciences, School of Medicine, National Yang-Ming University, Taipei, Taiwan;5. National Research Institute of Chinese Medicine, Taipei, Taiwan;6. Department and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan;7. Institute of Biopharmaceutical Sciences, School of Pharmacy, National Yang-Ming University, Taipei, Taiwan;8. Division of General Internal Medicine and Geriatrics, Department of Internal Medicine, Chang Gung Memorial Hospital at Linkou, Taoyuan City, Taiwan;9. Chang Gung University College of Medicine, Taoyuan City, Taiwan;10. Department of Toxicogenomics, National Institute of Public Health, Prague, Czech Republic;11. Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan;1. Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi''an 710032, China;2. Department of Geriatrics, Xijing Hospital, The Fourth Military Medical University, Xi''an 710032, China;3. Department of Physiology, The Fourth Military Medical University, Xi''an 710032, China |
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| Abstract: | Carotid atherosclerosis (AS) is an inflammatory process and is the primary pathogenesis of cerebrovascular disease. Many factors are responsible for development of atherosclerosis such as inflammation and autophagy. It is reported that microRNAs (miRNAs) could regulate the development of atherosclerosis through targeting autophagy-related genes. Many studies have demonstrated that miRNA-155 could regulate autophagy in macrophages or tumor cells. However, the role of miRNA-155 on autophagy in carotid plaques is not yet known. In this study, we explore the expression of miRNA-155 and autophagy-related proteins in carotid plaques of ApoE?/? mice and the interventional effect of rapamycin. We compared the expression of miRNA-155 and autophagy-related proteins between the control, model and rapamycin groups using qRT-PCR and western blot. Compared to the control group, we found the miRNA-155 and LC3-II expression was up-regulated (P < 0.05), expression ratio of phosphorylated mammalian target of rapamycin to total mammalian target of rapamycin (p-mTOR/mTOR) was down-regulated in model group (P < 0.05), but atherosclerotic lesions were still aggravated. These results following rapamycin group indicated that miRNA-155 and LC3-II expression was significantly up-regulated (P < 0.05), the expression ratio of p-mTOR/mTOR was significantly down-regulated (P < 0.05), and atherosclerotic lesions were reduced. Our results showed in the early stages of atherosclerotic plaques development, effective autophagy could attenuate atherosclerosis in ApoE?/? mice. Furthermore, our results also demonstrated that rapamycin might promote the activation of the autophagy by enhancing the expression of miRNA-155, which delays the development of atherosclerotic plaques. |
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