دورية أكاديمية

Investigating TIP30-Mediated regulation of mTORC1 signaling as a therapeutic strategy for coxsackievirus B3-Induced viral myocarditis.

التفاصيل البيبلوغرافية
العنوان: Investigating TIP30-Mediated regulation of mTORC1 signaling as a therapeutic strategy for coxsackievirus B3-Induced viral myocarditis.
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
الوصف
تدمد:1096-0341
DOI:10.1016/j.virol.2024.110156