Coxsackievirus B3 induces autophagy in HeLa cells via the AMPK/MEK/ERK and Ras/Raf/MEK/ERK signaling pathways |
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| Affiliation: | 1. Department of Obstetrics and Gynecology, Seoul St. Mary''s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea;2. Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea;3. Department of Occupational & Environmental Medicine, Seoul St. Mary''s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea;4. Department of Obstetrics and Gynecology, Uijeongbu St. Mary''s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea;1. Laboratory of Transmissible Diseases LR99-ES27, Faculty of Pharmacy, Avenue Avicenne 5000, Monastir, Tunisia;2. University of Vermont, Department of Pathology, Division of Experimental Pathology, Burlington, USA;3. University of Vermont, DNA Microarray Facility, 305 Health Science Research Facility, Burlington, USA;4. University of Vermont, Department of Pathology, 208 South Park Drive, Suite #2, Colchester, VT 05446, USA;1. Department of Microbiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People’s Republic of China;2. School of Health Sciences, Macao Polytechnic Institute, Macao SAR 999078, People’s Republic of China;1. Cardiac and Vascular Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea;2. Department of Biomedical Science, Jungwon University, Goesan-gun, South Korea;3. Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, South Korea;4. Center for Molecular & Cellular Imaging, Samsung Biomedical Research Institute, Seoul, South Korea;1. Department of Applied Biochemistry, Institute of Biotechnology, Technische Universität Berlin, Berlin, Germany;2. National Reference Centre for Poliomyelitis and Enteroviruses, Robert Koch Institute, Berlin, Germany;3. IQVD – Institut für Qualitätssicherung in der Virusdiagnostik, Berlin, Germany |
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| Abstract: | In a previous study, the number of autophagosomes increased after coxsackievirus B3 (CVB3) infection. However, the exact mechanism by which CVB3 regulates the number of autophagosomes is unclear. Earlier studies have found that infection with CVB3 activates extracellular signal-regulated kinase (ERK). ERK is essential for CVB3 replication and can increase the number of autophagosomes. In the current study, extracellular signal-regulated kinase 1/2 was activated in HeLa cells after CVB3 infection. The ERK kinase inhibitor, U0126, was then used to inhibit the activity of ERK. Treatment with U0126 led to a significant reduction in the number of autophagosomes indicating that the CVB3-induced autophagosome accumulation may have occurred via the ERK pathway. The relationship between CVB3 infection and ERK pathway activation was also investigated. The results showed that the RasGAP protein could be further cleaved, leading to the activation of the Ras/Raf/MEK (mitogen/extracellular signal-regulated kinase)/ERK pathway and that CVB3 infection could result in an increase in the concentration of calcium in the cytoplasm, resulting in mitochondrial damage, a decrease in the concentration of ATP and activation of the AMPK (AMP-activated protein kinase)/MEK/ERK pathway. In summary, CVB3 might directly or indirectly induce autophagy via AMPK/MEK/ERK and Ras/Raf/MEK/ERK signaling pathways in the host cells, representing a pivotal mechanism for CVB3 pathogenesis. |
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