Knowledge Management System of Hefei Institute of Physical Science，CAS
| TRIM32 Deficiency Impairs the Generation of Pyramidal Neurons in Developing Cerebral Cortex | |
| Sun, Yan-Yun1,2,3; Chen, Wen-Jin4,5; Huang, Ze-Ping1,2,3; Yang, Gang6; Wu, Ming-Lei1,2,3; Xu, De-En7; Yang, Wu-Lin8,9; Luo, Yong-Chun10; Xiao, Zhi-Cheng11; Xu, Ru-Xiang4,5; Ma, Quan-Hong1,2,3 | |
| 2022-02-01 | |
| Source Publication | CELLS
 |
| Corresponding Author | Xu, Ru-Xiang(xuruxiang1123@uestc.edu.cn) ; Ma, Quan-Hong(maquanhong@suda.edu.cn) |
| Abstract | Excitatory-inhibitory imbalance (E/I) is a fundamental mechanism underlying autism spectrum disorders (ASD). TRIM32 is a risk gene genetically associated with ASD. The absence of TRIM32 causes impaired generation of inhibitory GABAergic interneurons, neural network hyperexcitability, and autism-like behavior in mice, emphasizing the role of TRIM32 in maintaining E/I balance, but despite the description of TRIM32 in regulating proliferation and differentiation of cultured mouse neural progenitor cells (NPCs), the role of TRIM32 in cerebral cortical development, particularly in the production of excitatory pyramidal neurons, remains unknown. The present study observed that TRIM32 deficiency resulted in decreased numbers of distinct layer-specific cortical neurons and decreased radial glial cell (RGC) and intermediate progenitor cell (IPC) pool size. We further demonstrated that TRIM32 deficiency impairs self-renewal of RGCs and IPCs as indicated by decreased proliferation and mitosis. A TRIM32 deficiency also affects or influences the formation of cortical neurons. As a result, TRIM32-deficient mice showed smaller brain size. At the molecular level, RNAseq analysis indicated reduced Notch signalling in TRIM32-deficient mice. Therefore, the present study indicates a role for TRIM32 in pyramidal neuron generation. Impaired generation of excitatory pyramidal neurons may explain the hyperexcitability observed in TRIM32-deficient mice. |
| Keyword | TRIM32 excitatory-inhibitory imbalance cortex development ASD NPCs |
| DOI | 10.3390/cells11030449 |
| WOS Keyword | UPPER-LAYER NEURONS ; NEURAL STEM-CELLS ; HOXA1 ; DIFFERENTIATION ; PROLIFERATION ; ROLES ; PLASTICITY ; LEADS |
| Indexed By | SCI |
| Language | 英语 |
| WOS Research Area | Cell Biology |
| WOS Subject | Cell Biology |
| WOS ID | WOS:000759098700001 |
| Publisher | MDPI |
| Citation statistics | |
| Document Type | 期刊论文 |
| Identifier | http://ir.hfcas.ac.cn:8080/handle/334002/127486 |
| Collection | 中国科学院合肥物质科学研究院 |
| Corresponding Author | Xu, Ru-Xiang; Ma, Quan-Hong |
| Affiliation | 1.Soochow Univ, Dept Neurol, Affiliated Hosp 2, Suzhou 215123, Peoples R China 2.Soochow Univ, Clin Res Ctr Neurol Dis, Affiliated Hosp 2, Suzhou 215123, Peoples R China 3.Soochow Univ, Inst Neurosci, Jiangsu Key Lab Neuropsychiat Dis, Suzhou 215123, Peoples R China 4.Univ Elect Sci & Technol China, Sichuan Acad Med Sci, Dept Neurosurg, Chengdu 610072, Peoples R China 5.Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Chengdu 610072, Peoples R China 6.Soochow Univ, Lab Ctr, Coll Med, Suzhou 215123, Peoples R China 7.Wuxi 2 Peoples Hosp, Wuxi 214001, Peoples R China 8.Chinese Acad Sci, Anhui Prov Key Lab Med Phys & Technol, Inst Hlth & Med Technol, Hefei Inst Phys Sci, Hefei 230031, Peoples R China 9.Hefei Canc Hosp, Chinese Acad Sci, Hefei 230031, Peoples R China 10.Chinese Peoples Liberat Army Gen Hosp, Dept Neurosurg, Med Ctr 1, Beijing 100028, Peoples R China 11.Monash Univ, Dept Anat & Dev Biol, Clayton, Vic 3800, Australia |
| Recommended Citation GB/T 7714 | Sun, Yan-Yun,Chen, Wen-Jin,Huang, Ze-Ping,et al. TRIM32 Deficiency Impairs the Generation of Pyramidal Neurons in Developing Cerebral Cortex[J]. CELLS,2022,11. |
| APA | Sun, Yan-Yun.,Chen, Wen-Jin.,Huang, Ze-Ping.,Yang, Gang.,Wu, Ming-Lei.,...&Ma, Quan-Hong.(2022).TRIM32 Deficiency Impairs the Generation of Pyramidal Neurons in Developing Cerebral Cortex.CELLS,11. |
| MLA | Sun, Yan-Yun,et al."TRIM32 Deficiency Impairs the Generation of Pyramidal Neurons in Developing Cerebral Cortex".CELLS 11(2022). |
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