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2. SHFL inhibits enterovirus A71 infection by triggering degradation of viral 3Dpol protein via the ubiquitin–proteasome pathway

Author

Tan, Chahui, primary, Qin, Xingliang, additional, Tan, Yongyao, additional, Dong, Xinhuai, additional, Chen, Delin, additional, Liang, Linyue, additional, Li, Jinling, additional, Niu, Ruoxi, additional, Cao, Kaiyuan, additional, He, Zhenjian, additional, Wei, Guohong, additional, Huang, Mingxing, additional, and Zhu, Xun, additional

Published
2023
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4. SHFL inhibits enterovirus A71 infection by triggering degradation of viral 3Dpol protein via the ubiquitin–proteasome pathway.

Author

Tan, Chahui, Qin, Xingliang, Tan, Yongyao, Dong, Xinhuai, Chen, Delin, Liang, Linyue, Li, Jinling, Niu, Ruoxi, Cao, Kaiyuan, He, Zhenjian, Wei, Guohong, Huang, Mingxing, and Zhu, Xun

Subjects
ENTEROVIRUS diseases, VIRAL proteins, ORAL diseases, HAND, foot & mouth disease, LABORATORY mice, DNA polymerases
Abstract

Enterovirus A71 (EV‐A71) is a highly contagious virus that poses a major threat to global health, representing the primary etiological agent for hand–foot and mouth disease (HFMD) and neurological complications. It has been established that interferon signaling is critical to establishing a robust antiviral state in host cells, mainly mediated through the antiviral effects of numerous interferon‐stimulated genes (ISGs). The host restriction factor SHFL is a novel ISG with broad antiviral activity against various viruses through diverse underlying molecular mechanisms. Although SHFL is widely acknowledged for its broad‐spectrum antiviral activity, it remains elusive whether SHFL inhibits EV‐A71. In this work, we validated that EV‐A71 triggers the upregulation of SHFL both in cell lines and in a mouse model. Knockdown and overexpression of SHFL in EVA71‐infected cells suggested that this factor could markedly suppress EV‐A71 replication. Our findings further revealed an intriguing mechanism of SHFL that it could interact with the nonstructural proteins 3Dpol of EV‐A71 and promoted the degradation of 3Dpol through the ubiquitin–proteasome pathway. Furthermore, the zinc‐finger domain and the 36 amino acids (164–199) of SHFL were crucial to the interaction between SHFL and EV‐A71 3Dpol. Overall, these findings broadened our understanding of the pivotal roles of SHFL in the interaction between the host and EV‐A71. [ABSTRACT FROM AUTHOR]

Published
2023
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5. Neural progenitor cell pyroptosis contributes to Zika virus-induced brain atrophy and represents a therapeutic target

Author

Jie Yuan, Xun Zhu, Hengming Ye, Zhenjian He, Shuqing Zhang, Jueheng Wu, Yun Wu, Shu An, Mengfeng Li, Chen Jiahui, Jianchen Yu, and Tan Chahui

Subjects
Microcephaly, Multidisciplinary, Neurogenesis, Pyroptosis, Neuropathology, Biological Sciences, Biology, medicine.disease, biology.organism_classification, Neural stem cell, Zika virus, medicine, Progenitor cell, Neuroscience, Neural development
Abstract

Mounting evidence has associated Zika virus (ZIKV) infection with congenital malformations, including microcephaly, which raises global alarm. Nonetheless, mechanisms by which ZIKV disrupts neurogenesis and causes microcephaly are far from being understood. In this study, we discovered direct effects of ZIKV on neural progenitor cell development by inducing caspase-1– and gasdermin D (GSDMD)-mediated pyroptotic cell death, linking ZIKV infection with the development of microcephaly. Importantly, caspase-1 depletion or its inhibitor VX-765 treatment reduced ZIKV-induced inflammatory responses and pyroptosis, and substantially attenuated neuropathology and brain atrophy in vivo. Collectively, our data identify caspase-1– and GSDMD-mediated pyroptosis in neural progenitor cells as a previously unrecognized mechanism for ZIKV-related pathological effects during neural development, and also provide treatment options for ZIKV-associated diseases.

Published
2020

6. Tumour‐associated macrophages as a novel target of VEGI‐251 in cancer therapy

Author

Yun Wu, Tan Chahui, Zhicheng Yao, Jiajie Lin, Guohong Wei, Yiwen Hu, Jueheng Wu, Xun Zhu, Chen Delin, Xinhuai Dong, Xuan Huang, and Danrui Zhang

Subjects
Models, Molecular, 0301 basic medicine, TRAF2, Apoptosis, Immature Monocyte, law.invention, Mice, 0302 clinical medicine, law, ASK1 signalling, Neoplasms, Tumor-Associated Macrophages, Tumor Microenvironment, ASK1, Molecular Targeted Therapy, skin and connective tissue diseases, education.field_of_study, VEGI 251, Recombinant Proteins, Caspases, 030220 oncology & carcinogenesis, Recombinant DNA, Molecular Medicine, Original Article, Protein Binding, Signal Transduction, Tumor Necrosis Factor Ligand Superfamily Member 15, TAMs, Population, Antineoplastic Agents, Biology, Immunophenotyping, 03 medical and health sciences, stomatognathic system, Cell Line, Tumor, Animals, Humans, education, Cell Proliferation, Cancer prevention, Endothelial Cells, Original Articles, Cell Biology, Xenograft Model Antitumor Assays, In vitro, Disease Models, Animal, 030104 developmental biology, Cancer research, Carrier Proteins, Biomarkers
Abstract

Tumour‐associated macrophages (TAMs), which possess M2‐like characters and are derived from immature monocytes in the circulatory system, represent a predominant population of inflammatory cells in solid tumours. TAM infiltration in tumour microenvironment can be used as an important prognostic marker in many cancer types and is a potential target for cancer prevention or treatment. VEGI‐251 not only is involved in the inhibition of tumour angiogenesis, but also participates in the regulation of host immunity. This work aimed to investigate the involvement of VEGI‐251 in the regulation of specific antitumour immunity. We found that recombinant human VEGI‐251(rhVEGI‐251) efficiently mediated the elimination of TAMs in tumour tissue in mice, and induced apoptosis of purified TAMs in vitro. During this process, caspase‐8 and caspase‐3 were activated, leading to PARP cleavage and apoptosis. Most importantly, we further elucidated the mechanism underlying VEGI‐251‐triggered TAM apoptosis, which suggests that ASK1, an intermediate component of the VEGI‐251, activates the JNK pathway via TRAF2 in a potentially DR3‐dependent manner in the process of TAM apoptosis. Collectively, our findings provide new insights into the basic mechanisms underlying the actions of VEGI‐251 that might lead to future development of antitumour therapeutic strategies using VEGI‐251 to target TAMs.

Published
2020

8. SHFL inhibits enterovirus A71 infection by triggering degradation of viral 3D pol protein via the ubiquitin-proteasome pathway.

Author

Tan C, Qin X, Tan Y, Dong X, Chen D, Liang L, Li J, Niu R, Cao K, He Z, Wei G, Huang M, and Zhu X

Subjects
Animals, Mice, Proteasome Endopeptidase Complex, Gene Products, pol, Antigens, Viral genetics, Antiviral Agents, Interferons, Ubiquitins, Enterovirus A, Human genetics, Enterovirus Infections, Enterovirus, Hand, Foot and Mouth Disease
Abstract

Enterovirus A71 (EV-A71) is a highly contagious virus that poses a major threat to global health, representing the primary etiological agent for hand-foot and mouth disease (HFMD) and neurological complications. It has been established that interferon signaling is critical to establishing a robust antiviral state in host cells, mainly mediated through the antiviral effects of numerous interferon-stimulated genes (ISGs). The host restriction factor SHFL is a novel ISG with broad antiviral activity against various viruses through diverse underlying molecular mechanisms. Although SHFL is widely acknowledged for its broad-spectrum antiviral activity, it remains elusive whether SHFL inhibits EV-A71. In this work, we validated that EV-A71 triggers the upregulation of SHFL both in cell lines and in a mouse model. Knockdown and overexpression of SHFL in EVA71-infected cells suggested that this factor could markedly suppress EV-A71 replication. Our findings further revealed an intriguing mechanism of SHFL that it could interact with the nonstructural proteins 3D pol of EV-A71 and promoted the degradation of 3D pol through the ubiquitin-proteasome pathway. Furthermore, the zinc-finger domain and the 36 amino acids (164-199) of SHFL were crucial to the interaction between SHFL and EV-A71 3D pol . Overall, these findings broadened our understanding of the pivotal roles of SHFL in the interaction between the host and EV-A71., (© 2023 Wiley Periodicals LLC.)

Published
2023
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