Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity
Abstract Lipid metabolism has been considered as a potential therapeutic target in sevoflurane‐induced neurotoxicity that can potentially affect the learning and memory function in the developmental brain. Recently, triggering receptor expressed on myeloid cells 2 (TREM2) is identified as a crucial...
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| Format: | Article |
| Language: | English |
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Wiley
2024-03-01
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| Series: | Advanced Science |
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| Online Access: | https://doi.org/10.1002/advs.202305989 |
| _version_ | 1797263448665489408 |
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| author | Wenting Li Xiaowen Meng Ke Peng Yaobao Han Hanghang Liu Weiming Zhao Gang Wang Li Deng Hong Liu Zhen Li Fuhai Ji |
| author_facet | Wenting Li Xiaowen Meng Ke Peng Yaobao Han Hanghang Liu Weiming Zhao Gang Wang Li Deng Hong Liu Zhen Li Fuhai Ji |
| author_sort | Wenting Li |
| collection | DOAJ |
| description | Abstract Lipid metabolism has been considered as a potential therapeutic target in sevoflurane‐induced neurotoxicity that can potentially affect the learning and memory function in the developmental brain. Recently, triggering receptor expressed on myeloid cells 2 (TREM2) is identified as a crucial step in regulating lipid metabolism and associated with the pathogenesis of neurodegenerative diseases. Herein, it is reported that quercetin modified Cu2‐xSe (abbreviated as CSPQ) nanoparticles can ameliorate sevoflurane‐induced neurotoxicity by tuning the microglial lipid metabolism and promoting microglial M2‐like polarization via TREM2 signaling pathway, in which the apolipoprotein E (ApoE), and adenosine triphosphate‐binding cassette transporters (ABCA1 and ABCG1) levels are upregulated. Furthermore, the protective effects of CSPQ nanoparticles against sevoflurane‐induced neurotoxicity via TREM2 are further demonstrated by the small interfering RNA (siRNA)‐TREM2 transfected BV2 cells, which are obviously not influenced by CSPQ nanoparticles. The cell membrane coated CSPQ (referred as CSPQ@CM) nanoparticles can significantly reduce sevoflurane‐induced learning and memory deficits, improve lipid metabolism dysfunction, and promote the remyelination in the hippocampus of mice. The study shows great potential of targeting microglial lipid metabolism in promoting remyelination of neurons for treatment of neurotoxicity and neurodegenerative diseases. |
| first_indexed | 2024-04-25T00:13:10Z |
| format | Article |
| id | doaj.art-290ce76edd594be2954d8a9f379b1606 |
| institution | Directory Open Access Journal |
| issn | 2198-3844 |
| language | English |
| last_indexed | 2024-04-25T00:13:10Z |
| publishDate | 2024-03-01 |
| publisher | Wiley |
| record_format | Article |
| series | Advanced Science |
| spelling | doaj.art-290ce76edd594be2954d8a9f379b16062024-03-13T07:30:35ZengWileyAdvanced Science2198-38442024-03-011110n/an/a10.1002/advs.202305989Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental NeurotoxicityWenting Li0Xiaowen Meng1Ke Peng2Yaobao Han3Hanghang Liu4Weiming Zhao5Gang Wang6Li Deng7Hong Liu8Zhen Li9Fuhai Ji10Department of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaDepartment of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaDepartment of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaCenter for Molecular Imaging and Nuclear Medicine State Key Laboratory of Radiation Medicine and Protection School for Radiological and Interdisciplinary Sciences (RAD‐X) Suzhou Medical College Soochow University Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions Suzhou 215123 ChinaCenter for Molecular Imaging and Nuclear Medicine State Key Laboratory of Radiation Medicine and Protection School for Radiological and Interdisciplinary Sciences (RAD‐X) Suzhou Medical College Soochow University Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions Suzhou 215123 ChinaDepartment of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaDepartment of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaDepartment of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaDepartment of Anaesthesiology and Pain Medicine University of California Davis Health Sacramento CA 95817 USACenter for Molecular Imaging and Nuclear Medicine State Key Laboratory of Radiation Medicine and Protection School for Radiological and Interdisciplinary Sciences (RAD‐X) Suzhou Medical College Soochow University Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions Suzhou 215123 ChinaDepartment of Anesthesiology the First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 ChinaAbstract Lipid metabolism has been considered as a potential therapeutic target in sevoflurane‐induced neurotoxicity that can potentially affect the learning and memory function in the developmental brain. Recently, triggering receptor expressed on myeloid cells 2 (TREM2) is identified as a crucial step in regulating lipid metabolism and associated with the pathogenesis of neurodegenerative diseases. Herein, it is reported that quercetin modified Cu2‐xSe (abbreviated as CSPQ) nanoparticles can ameliorate sevoflurane‐induced neurotoxicity by tuning the microglial lipid metabolism and promoting microglial M2‐like polarization via TREM2 signaling pathway, in which the apolipoprotein E (ApoE), and adenosine triphosphate‐binding cassette transporters (ABCA1 and ABCG1) levels are upregulated. Furthermore, the protective effects of CSPQ nanoparticles against sevoflurane‐induced neurotoxicity via TREM2 are further demonstrated by the small interfering RNA (siRNA)‐TREM2 transfected BV2 cells, which are obviously not influenced by CSPQ nanoparticles. The cell membrane coated CSPQ (referred as CSPQ@CM) nanoparticles can significantly reduce sevoflurane‐induced learning and memory deficits, improve lipid metabolism dysfunction, and promote the remyelination in the hippocampus of mice. The study shows great potential of targeting microglial lipid metabolism in promoting remyelination of neurons for treatment of neurotoxicity and neurodegenerative diseases.https://doi.org/10.1002/advs.202305989biomimetic nanoparticleslipid metabolismneuroinflammationsevoflurane‐induced neurotoxicityTREM2 |
| spellingShingle | Wenting Li Xiaowen Meng Ke Peng Yaobao Han Hanghang Liu Weiming Zhao Gang Wang Li Deng Hong Liu Zhen Li Fuhai Ji Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity Advanced Science biomimetic nanoparticles lipid metabolism neuroinflammation sevoflurane‐induced neurotoxicity TREM2 |
| title | Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity |
| title_full | Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity |
| title_fullStr | Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity |
| title_full_unstemmed | Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity |
| title_short | Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane‐Induced Developmental Neurotoxicity |
| title_sort | boosting microglial lipid metabolism via trem2 signaling by biomimetic nanoparticles to attenuate the sevoflurane induced developmental neurotoxicity |
| topic | biomimetic nanoparticles lipid metabolism neuroinflammation sevoflurane‐induced neurotoxicity TREM2 |
| url | https://doi.org/10.1002/advs.202305989 |
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