MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1
Abstract Background Rotavirus (RV) is the main cause of serious diarrhea in infants and young children worldwide. Numerous studies have demonstrated that RV use host cell mechanisms to motivate their own stabilization and multiplication by degrading, enhancing, or hijacking microRNAs (miRNAs). There...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2023-09-01
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| Series: | Virology Journal |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12985-023-02175-z |
| _version_ | 1797453911515201536 |
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| author | Haohai Huang Dan Liao Guanghui Zhou Bin He Rong Pu Yejia Cui |
| author_facet | Haohai Huang Dan Liao Guanghui Zhou Bin He Rong Pu Yejia Cui |
| author_sort | Haohai Huang |
| collection | DOAJ |
| description | Abstract Background Rotavirus (RV) is the main cause of serious diarrhea in infants and young children worldwide. Numerous studies have demonstrated that RV use host cell mechanisms to motivate their own stabilization and multiplication by degrading, enhancing, or hijacking microRNAs (miRNAs). Therefore, exploring the molecular mechanisms by which miRNAs motivate or restrain RV replication by controlling different biological processes, including autophagy, will help to better understand the pathogenesis of RV development. This study mainly explored the effect of miR-194-3p on autophagy after RV infection and its underlying mechanism of the regulation of RV replication. Methods Caco-2 cells were infected with RV and used to measure the expression levels of miR-194-3p and silent information regulator 1 (SIRT1). After transfection with plasmids and RV infection, viral structural proteins, RV titer, cell viability, and autophagy-linked proteins were tested. The degree of acetylation of p53 was further investigated. A RV-infected neonatal mouse model was constructed in vivo and was evaluated for diarrhea symptoms and lipid droplet formation. Results The results showed that miR-194-3p was reduced but SIRT1 was elevated after RV infection. Elevation of miR-194-3p or repression of SIRT1 inhibited RV replication through the regulation of autophagy. The overexpression of SIRT1 reversed the effects of miR-194-3p on RV replication. The upregulation of miR-194-3p or the downregulation of SIRT1 repressed RV replication in vivo. MiR-194-3p targeted SIRT1 to decrease p53 acetylation. Conclusion These results were used to determine the mechanism of miR-194-3p in RV replication, and identified a novel therapeutic small RNA molecule that can be used against RV. |
| first_indexed | 2024-03-09T15:29:41Z |
| format | Article |
| id | doaj.art-e184ac4bb4f44bd1bc71e5d210c41d0b |
| institution | Directory Open Access Journal |
| issn | 1743-422X |
| language | English |
| last_indexed | 2024-03-09T15:29:41Z |
| publishDate | 2023-09-01 |
| publisher | BMC |
| record_format | Article |
| series | Virology Journal |
| spelling | doaj.art-e184ac4bb4f44bd1bc71e5d210c41d0b2023-11-26T12:20:37ZengBMCVirology Journal1743-422X2023-09-0120111110.1186/s12985-023-02175-zMicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1Haohai Huang0Dan Liao1Guanghui Zhou2Bin He3Rong Pu4Yejia Cui5Department of Clinical Pharmacy, SSL Central Hospital of Dongguan, Dongguan Third People’s Hospital, Affiliated Dongguan Shilong People’s Hospital of Southern Medical UniversityDepartment of Gynaecology, SSL Central Hospital of Dongguan, Dongguan Third People’s Hospital, Affiliated Dongguan Shilong People’s Hospital of Southern Medical UniversityDepartment of Rehabilitation medicine, SSL Central Hospital of Dongguan, Dongguan Third People’s Hospital, Affiliated Dongguan Shilong People’s Hospital of Southern Medical UniversityMedical and Pharmacy Research Laboratory, SSL Central Hospital of Dongguan, Dongguan Third People’s Hospital, Affiliated Dongguan Shilong People’s Hospital of Southern Medical UniversityDepartment of Clinical Laboratory, SSL Central Hospital of Dongguan, Dongguan Third People’s Hospital, Affiliated Dongguan Shilong People’s Hospital of Southern Medical UniversityDepartment of Clinical Laboratory, SSL Central Hospital of Dongguan, Dongguan Third People’s Hospital, Affiliated Dongguan Shilong People’s Hospital of Southern Medical UniversityAbstract Background Rotavirus (RV) is the main cause of serious diarrhea in infants and young children worldwide. Numerous studies have demonstrated that RV use host cell mechanisms to motivate their own stabilization and multiplication by degrading, enhancing, or hijacking microRNAs (miRNAs). Therefore, exploring the molecular mechanisms by which miRNAs motivate or restrain RV replication by controlling different biological processes, including autophagy, will help to better understand the pathogenesis of RV development. This study mainly explored the effect of miR-194-3p on autophagy after RV infection and its underlying mechanism of the regulation of RV replication. Methods Caco-2 cells were infected with RV and used to measure the expression levels of miR-194-3p and silent information regulator 1 (SIRT1). After transfection with plasmids and RV infection, viral structural proteins, RV titer, cell viability, and autophagy-linked proteins were tested. The degree of acetylation of p53 was further investigated. A RV-infected neonatal mouse model was constructed in vivo and was evaluated for diarrhea symptoms and lipid droplet formation. Results The results showed that miR-194-3p was reduced but SIRT1 was elevated after RV infection. Elevation of miR-194-3p or repression of SIRT1 inhibited RV replication through the regulation of autophagy. The overexpression of SIRT1 reversed the effects of miR-194-3p on RV replication. The upregulation of miR-194-3p or the downregulation of SIRT1 repressed RV replication in vivo. MiR-194-3p targeted SIRT1 to decrease p53 acetylation. Conclusion These results were used to determine the mechanism of miR-194-3p in RV replication, and identified a novel therapeutic small RNA molecule that can be used against RV.https://doi.org/10.1186/s12985-023-02175-zRotavirusMicroRNA-194-3pSilent information regulator 1Viral replicationAutophagyp53 acetylation |
| spellingShingle | Haohai Huang Dan Liao Guanghui Zhou Bin He Rong Pu Yejia Cui MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 Virology Journal Rotavirus MicroRNA-194-3p Silent information regulator 1 Viral replication Autophagy p53 acetylation |
| title | MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 |
| title_full | MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 |
| title_fullStr | MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 |
| title_full_unstemmed | MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 |
| title_short | MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 |
| title_sort | microrna 194 3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1 |
| topic | Rotavirus MicroRNA-194-3p Silent information regulator 1 Viral replication Autophagy p53 acetylation |
| url | https://doi.org/10.1186/s12985-023-02175-z |
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