The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells
Abstract The transient receptor potential vanilloid 2 (TRPV2) channel is a nonselective cation channel that has been implicated in multiple sensory processes in the nervous system. Here, it is shown that TRPV2 in myeloid cells facilitates virus penetration by promoting the tension and mobility of ce...
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| Format: | Article |
| Language: | English |
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Wiley
2022-12-01
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| Series: | Advanced Science |
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| Online Access: | https://doi.org/10.1002/advs.202202857 |
| _version_ | 1811178425081135104 |
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| author | Yu‐Yao Guo Yue Gao Yu‐Ru Hu Yuhan Zhao Dexiang Jiang Yulin Wang Youjing Zhang Hu Gan Chang Xie Zheng Liu Bo Zhong Zhi‐Dong Zhang Jing Yao |
| author_facet | Yu‐Yao Guo Yue Gao Yu‐Ru Hu Yuhan Zhao Dexiang Jiang Yulin Wang Youjing Zhang Hu Gan Chang Xie Zheng Liu Bo Zhong Zhi‐Dong Zhang Jing Yao |
| author_sort | Yu‐Yao Guo |
| collection | DOAJ |
| description | Abstract The transient receptor potential vanilloid 2 (TRPV2) channel is a nonselective cation channel that has been implicated in multiple sensory processes in the nervous system. Here, it is shown that TRPV2 in myeloid cells facilitates virus penetration by promoting the tension and mobility of cell membrane through the Ca2+‐LRMDA axis. Knockout of TRPV2 in myeloid cells or inhibition of TRPV2 channel activity suppresses viral infection and protects mice from herpes simplex virus 1 (HSV‐1) and vesicular stomatitis virus (VSV) infection. Reconstitution of TRPV2 but not the Ca2+‐impermeable mutant TRPV2E572Q into LyZ2‐Cre;Trpv2fl/fl bone marrow‐derived dendritic cells (BMDCs) restores viral infection. Mechanistically, knockout of TRPV2 in myeloid cells inhibits the tension and mobility of cell membrane and the penetration of viruses, which is restored by reconstitution of TRPV2 but not TRPV2E572Q. In addition, knockout of TRPV2 leads to downregulation of Lrmda in BMDCs and BMDMs, and knockdown of Lrmda significantly downregulates the mobility and tension of cell membrane and inhibits viral infections in Trpv2fl/fl but not LyZ2‐Cre;Trpv2fl/fl BMDCs. Consistently, complement of LRMDA into LyZ2‐Cre;Trpv2fl/fl BMDCs partially restores the tension and mobility of cell membrane and promotes viral penetration and infection. These findings characterize a previously unknown function of myeloid TRPV2 in facilitating viral infection though the Ca2+‐LRMDA axis. |
| first_indexed | 2024-04-11T06:18:04Z |
| format | Article |
| id | doaj.art-03cc88464caa4314bd9799f23ecb58bf |
| institution | Directory Open Access Journal |
| issn | 2198-3844 |
| language | English |
| last_indexed | 2024-04-11T06:18:04Z |
| publishDate | 2022-12-01 |
| publisher | Wiley |
| record_format | Article |
| series | Advanced Science |
| spelling | doaj.art-03cc88464caa4314bd9799f23ecb58bf2022-12-22T04:40:58ZengWileyAdvanced Science2198-38442022-12-01934n/an/a10.1002/advs.202202857The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid CellsYu‐Yao Guo0Yue Gao1Yu‐Ru Hu2Yuhan Zhao3Dexiang Jiang4Yulin Wang5Youjing Zhang6Hu Gan7Chang Xie8Zheng Liu9Bo Zhong10Zhi‐Dong Zhang11Jing Yao12Department of Gastrointestinal Surgery College of Life Sciences Zhongnan Hospital of Wuhan University Wuhan University Wuhan 430071 ChinaDepartment of Gastrointestinal Surgery College of Life Sciences Zhongnan Hospital of Wuhan University Wuhan University Wuhan 430071 ChinaThe Institute for Advanced Studies Wuhan University Wuhan 430072 ChinaState Key Laboratory of Virology Hubei Key Laboratory of Cell Homeostasis College of Life Sciences Frontier Science Center for Immunology and Metabolism Wuhan University Wuhan 430072 ChinaState Key Laboratory of Virology Hubei Key Laboratory of Cell Homeostasis College of Life Sciences Frontier Science Center for Immunology and Metabolism Wuhan University Wuhan 430072 ChinaState Key Laboratory of Virology Hubei Key Laboratory of Cell Homeostasis College of Life Sciences Frontier Science Center for Immunology and Metabolism Wuhan University Wuhan 430072 ChinaState Key Laboratory of Virology Hubei Key Laboratory of Cell Homeostasis College of Life Sciences Frontier Science Center for Immunology and Metabolism Wuhan University Wuhan 430072 ChinaDepartment of Gastrointestinal Surgery College of Life Sciences Zhongnan Hospital of Wuhan University Wuhan University Wuhan 430071 ChinaState Key Laboratory of Virology Hubei Key Laboratory of Cell Homeostasis College of Life Sciences Frontier Science Center for Immunology and Metabolism Wuhan University Wuhan 430072 ChinaThe Institute for Advanced Studies Wuhan University Wuhan 430072 ChinaDepartment of Gastrointestinal Surgery College of Life Sciences Zhongnan Hospital of Wuhan University Wuhan University Wuhan 430071 ChinaDepartment of Gastrointestinal Surgery College of Life Sciences Zhongnan Hospital of Wuhan University Wuhan University Wuhan 430071 ChinaDepartment of Gastrointestinal Surgery College of Life Sciences Zhongnan Hospital of Wuhan University Wuhan University Wuhan 430071 ChinaAbstract The transient receptor potential vanilloid 2 (TRPV2) channel is a nonselective cation channel that has been implicated in multiple sensory processes in the nervous system. Here, it is shown that TRPV2 in myeloid cells facilitates virus penetration by promoting the tension and mobility of cell membrane through the Ca2+‐LRMDA axis. Knockout of TRPV2 in myeloid cells or inhibition of TRPV2 channel activity suppresses viral infection and protects mice from herpes simplex virus 1 (HSV‐1) and vesicular stomatitis virus (VSV) infection. Reconstitution of TRPV2 but not the Ca2+‐impermeable mutant TRPV2E572Q into LyZ2‐Cre;Trpv2fl/fl bone marrow‐derived dendritic cells (BMDCs) restores viral infection. Mechanistically, knockout of TRPV2 in myeloid cells inhibits the tension and mobility of cell membrane and the penetration of viruses, which is restored by reconstitution of TRPV2 but not TRPV2E572Q. In addition, knockout of TRPV2 leads to downregulation of Lrmda in BMDCs and BMDMs, and knockdown of Lrmda significantly downregulates the mobility and tension of cell membrane and inhibits viral infections in Trpv2fl/fl but not LyZ2‐Cre;Trpv2fl/fl BMDCs. Consistently, complement of LRMDA into LyZ2‐Cre;Trpv2fl/fl BMDCs partially restores the tension and mobility of cell membrane and promotes viral penetration and infection. These findings characterize a previously unknown function of myeloid TRPV2 in facilitating viral infection though the Ca2+‐LRMDA axis.https://doi.org/10.1002/advs.202202857antiviral immunityCa2+ influxLrmdamyeloid cellsTRPV2virus penetration |
| spellingShingle | Yu‐Yao Guo Yue Gao Yu‐Ru Hu Yuhan Zhao Dexiang Jiang Yulin Wang Youjing Zhang Hu Gan Chang Xie Zheng Liu Bo Zhong Zhi‐Dong Zhang Jing Yao The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells Advanced Science antiviral immunity Ca2+ influx Lrmda myeloid cells TRPV2 virus penetration |
| title | The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells |
| title_full | The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells |
| title_fullStr | The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells |
| title_full_unstemmed | The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells |
| title_short | The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells |
| title_sort | transient receptor potential vanilloid 2 trpv2 channel facilitates virus infection through the ca2 lrmda axis in myeloid cells |
| topic | antiviral immunity Ca2+ influx Lrmda myeloid cells TRPV2 virus penetration |
| url | https://doi.org/10.1002/advs.202202857 |
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