دورية أكاديمية
Activation of α7 nicotinic acetylcholine receptor promotes HIV-1 transcription.
| العنوان: | Activation of α7 nicotinic acetylcholine receptor promotes HIV-1 transcription. |
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| المؤلفون: | Wen J; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Zhao C; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Chen J; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Song S; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Lin Z; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Xie S; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Qi H; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China., Wang J; Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510670, China., Su X; Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, 200031, China.; University of Chinese Academy of Sciences, Beijing, 100049, China. |
| المصدر: | Cell insight [Cell Insight] 2022 Apr 27; Vol. 1 (3), pp. 100028. Date of Electronic Publication: 2022 Apr 27 (Print Publication: 2022). |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier B.V Country of Publication: Netherlands NLM ID: 9918557775706676 Publication Model: eCollection Cited Medium: Internet ISSN: 2772-8927 (Electronic) Linking ISSN: 27728927 NLM ISO Abbreviation: Cell Insight Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: [Amsterdam] : Elsevier B.V., 2022- |
| مستخلص: | Alpha7 nicotinic acetylcholine receptor (α7 nAChR), a hub of the cholinergic anti-inflammatory pathway (CAP), is required for the treatment of inflammatory diseases. HIV-1 infection can upregulate the expression of α7 nAChR in T lymphocytes and affect the role of CAP. However, whether α7 nAChR regulates HIV-1 infection in CD4 + T cells is unclear. In this study, we first found that activation of α7 nAChR by GTS-21 (an α7 nAChR agonist) can promote the transcription of HIV-1 proviral DNA. Then, through transcriptome sequencing analysis, we found that p38 MAPK signaling was enriched in GTS-21 treated HIV-latent T cells. Mechanistically, activation of α7 nAChR could increase reactive oxygen species (ROS), reduce DUSP1 and DUSP6 , and consequently enhance the phosphorylation of p38 MAPK. By co-immunoprecipitation and liquid chromatography tandem mass spectrometry, we found that p-p38 MAPK interacted with Lamin B1 (LMNB1). Activation of α7 nAChR increased the binding between p-p38 MAPK and LMNB1. We confirmed that knockdown of MAPK14 significantly downregulated NFATC4, a key activator of HIV-1 transcription. Taken together, activation of the α7 nAChR could trigger ROS/p-p38 MAPK/LMNB1/NFATC4 signaling pathway enhancing HIV-1 transcription. We have revealed an unrecognized mechanism of α7 nAChR-mediated neuroimmune regulation of HIV infection. Competing Interests: The authors have declared that no competing interests exist. (© 2022 The Authors.) |
| فهرسة مساهمة: | Keywords: HIV-1; LMNB1; ROS; p38 MAPK; α7 nAChR |
| تواريخ الأحداث: | Date Created: 20230516 Latest Revision: 20230920 |
| رمز التحديث: | 20240829 |
| مُعرف محوري في PubMed: | PMC10120325 |
| DOI: | 10.1016/j.cellin.2022.100028 |
| PMID: | 37193048 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2772-8927 |
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| DOI: | 10.1016/j.cellin.2022.100028 |