ROCK is Involved in Vimentin Phosphorylation and Rearrangement Induced by Dengue Virus |
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Authors: | Shun Lei Yan-Ping Tian Wei-Dong Xiao Shu Li Xian-Cai Rao Jun-Lei Zhang Jie Yang Xiao-Mei Hu Wei Chen |
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Affiliation: | 1. Department of Microbiology, Third Military Medical University, Chongqing, 400038, People’s Republic of China 2. Department of Histology and Embryology, Third Military Medical University, Chongqing, 400038, People’s Republic of China 3. Department of General Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, People’s Republic of China
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Abstract: | Our previous study showed that dengue virus 2 (DENV2) infection induces rearrangement of vimentin into dense structures at the perinuclear area. However, the underlying mechanism of this phenomenon is poorly characterized. In the present work, we found that vimentin and Ser71 phosphorylated vimentin display similar distributions in DENV2-infected cells. DENV2 infection also induced ROCK activation and phosphorylation of vimentin at Ser71 as the DENV2 infection progressed. Furthermore, Ser71 phosphorylation and vimentin rearrangement induced by DENV2 infection were blocked by the ROCK inhibitor Y-27632. In addition, DENV2 led to endoplasmic reticulum (ER) redistribution in the perinuclear region of the host cells, which was partially blocked by pretreatment with Y-27632. Together, these data support indicate that ROCK may have a role in governing regulating vimentin and ER rearrangement during DENV2 infection. We hypothesize that DENV2 infection, via ROCK activation, induces both vimentin rearrangement and ER redistribution around the perinuclear region, which may play a structural role in anchoring DENV2 to replication sites. |
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