دورية أكاديمية
Investigating TIP30-Mediated regulation of mTORC1 signaling as a therapeutic strategy for coxsackievirus B3-Induced viral myocarditis.
العنوان: | Investigating TIP30-Mediated regulation of mTORC1 signaling as a therapeutic strategy for coxsackievirus B3-Induced viral myocarditis. |
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المؤلفون: | Liu XL; Cardiovascular Medicine, Xinxiang Central Hospital, Xinxiang, 453000, Henan, China., Hou YY; Cardiovascular Medicine, Xinxiang Central Hospital, Xinxiang, 453000, Henan, China., Su SH; Cardiovascular Medicine, Xinxiang Central Hospital, Xinxiang, 453000, Henan, China., Wu X; Cardiovascular Medicine, Xinxiang Central Hospital, Xinxiang, 453000, Henan, China., Wang ZF; Cardiovascular Medicine, Xinxiang Central Hospital, Xinxiang, 453000, Henan, China. Electronic address: wangzhifang1964@163.com. |
المصدر: | Virology [Virology] 2024 Sep; Vol. 597, pp. 110156. Date of Electronic Publication: 2024 Jun 21. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Academic Press Country of Publication: United States NLM ID: 0110674 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1096-0341 (Electronic) Linking ISSN: 00426822 NLM ISO Abbreviation: Virology Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: New York, Academic Press. |
مواضيع طبية MeSH: | Coxsackievirus Infections*/virology , Coxsackievirus Infections*/metabolism , Enterovirus B, Human*/physiology , Mechanistic Target of Rapamycin Complex 1*/metabolism , Mice, Knockout* , Myocarditis*/virology , Myocarditis*/metabolism , Signal Transduction*, Animals ; Humans ; Male ; Mice ; Disease Models, Animal ; HeLa Cells ; Transcription Factors/metabolism ; Transcription Factors/genetics ; Virus Replication |
مستخلص: | This study aims to elucidate the role of TIP30 (30 KDa HIV-1 TAT-Interacting Protein) in the progression of coxsackievirus B3 (CVB3)-induced viral myocarditis. TIP30 knockout and wildtype mice were intraperitoneally infected with CVB3 and evaluated at day 7 post-infection. HeLa cells were transfected with TIP30 lentiviral particles and subsequently infected with CVB3 to evaluate viral replication, cellular pathogenesis, and mechanistic target of rapamycin complex 1 (mTORC1) signaling. Deletion of the TIP30 gene heightened heart virus titers and mortality rates in mice with CVB3-induced myocarditis, exacerbating cardiac damage and fibrosis, and elevating pro-inflammatory factors level. In vitro experiments demonstrated the modulation of mTORC1 signaling by TIP30 during CVB3 infection in HeLa cells. TIP30 overexpression mitigated CVB3-induced cellular pathogenesis and VP1 expression, with rapamycin, an mTOR1 inhibitor, reversing these effects. These findings suggest TIP30 plays a critical protective role against CVB3-induced myocarditis by regulating mTORC1 signaling. Competing Interests: Declaration of competing interest The authors declare that they have no competing interests. (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.) |
فهرسة مساهمة: | Keywords: 30 KDa HIV-1 TAT-Interacting protein; Coxsackievirus B3; Viral myocarditis; mTORC1 signaling |
المشرفين على المادة: | EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1) 0 (Transcription Factors) 0 (Tip30 protein, mouse) |
تواريخ الأحداث: | Date Created: 20240709 Date Completed: 20240718 Latest Revision: 20240819 |
رمز التحديث: | 20240819 |
DOI: | 10.1016/j.virol.2024.110156 |
PMID: | 38981316 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1096-0341 |
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DOI: | 10.1016/j.virol.2024.110156 |