Zhaocong Wei

Nanjing Medical University

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Xiang Chen

Northeast Agricultural University

Ying‐Mei Lu

Nanjing Medical University

Feng Han

Ministry of Education of the People's Republic of China

Xiuxiu Liu

Nanjing Medical University

Takuya Sasaki

University of California, San Diego

Ya-Ping Lu

Hangzhou Dianzi University

Da Huo

Nanjing Medical University

Li Zhang

University of California, San Francisco

Guojun Jiang

The First People's Hospital of Xiaoshan District, Hangzhou

Weifeng Ye

Children's Hospital of Zhejiang University

Cooperative Institutions

Nanjing Medical University

Zhejiang University

Capital Medical University

Second Affiliated Hospital of Nanjing Medical University

Suzhou Municipal Hospital

Ministry of Education of the People's Republic of China

Chinese Academy of Medical Sciences & Peking Union Medical College

Jiangsu Province Hospital

Chinese Academy of Sciences

Nanjing Brain Hospital

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Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice

MedComm (2022)

Zheng‐Mao Li Xiuxiu Liu Chen Li Zhaocong Wei Yi Shi

Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal-dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome-wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy-related genes, there are changes in synaptic organization pathway node genes, such as

Memory Impairment

10.1002/mco2.128

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Discussion on the mechanism of glial scar inhibiting axonal regeneration in CNS and new techniques of anti-inhibition regeneration

Highlights in Science Engineering and Technology (2023)

Zhaocong Wei

Nerve regeneration is a process of self-recovery after nerve injury. Nerve regeneration is more difficult in the central nervous system (CNS) than in the peripheral nervous system (PNS). So far, there are few cases of CNS cure. The difficulty of CNS regeneration brings great loss to patients and society. In recent years, scientific research has found that damage to the CNS is caused by mechanisms that hinder its regeneration. This review has provided a comprehensive summary of recent studies on the inhibitory mechanism of glial scar, which are the main factors affecting axonal regeneration in the CNS, and deeply discussed the mechanism of a series of factors related to glial scar, such as CSPGs, Nogo family proteins, NgR1, LINGO-1 and p75, on the production of glial scar. After this, the idea of their ability to study the regeneration of the CNS after injury was analyzed, and the new technology of anti-inhibition of CNS regeneration therapy was looked forward.

Glial scar

Peripheral Nervous System

10.54097/hset.v36i.6183

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Endothelial TFEB signaling-mediated autophagic disturbance initiates microglial activation and cognitive dysfunction

Autophagy (2023)

Ya-Ping Lu Xiang Chen Xiuxiu Liu Yi Shi Zhaocong Wei

Cognitive impairment caused by systemic chemotherapy is a critical question that perplexes the effective implementation of clinical treatment, but related molecular events are poorly understood. Herein, we show that bortezomib exposure leads to microglia activation and cognitive impairment, this occurs along with decreased nuclear translocation of TFEB (transcription factor EB), which is linked to macroautophagy/autophagy disorder, STAT3 (signal transducer and activator of transcription 3) phosphorylation and IL23A (interleukin 23 subunit alpha) expression. Pharmacological enhancement of TFEB nuclear translocation by digoxin restores lysosomal function and reduces STAT3-dependent endothelial IL23A secretion. As a consequence, we found that brain endothelial-specific ablation of Il23a ameliorated both microglia activation and cognitive dysfunction. Thus, the endothelial TFEB-STAT3-IL23A axis in the brain represents a critical cellular event for initiating bortezomib-mediated aberrant microglial activation and synapse engulfment. Our results suggest the reversal of TFEB nuclear translocation may provide a novel therapeutic approach to prevent symptoms of cognitive dysfunction during clinical use of bortezomib.Abbreviations: AAV: adeno-associated virus; BBB: blood-brain barrier; BTZ: bortezomib; DG: digoxin; DGs: dentate gyrus; DLG4/PSD95: discs large MAGUK scaffold protein 4; HBMECs: human brain microvascular endothelial cells; HP: hippocampus; IL23A: interleukin 23 subunit alpha; MBVECs: mouse brain vascular endothelial cells; mPFC: medial prefrontal cortex; NORT: novel object recognition test; OLT: object location test; PLX5622: 6-fluoro-N-([5-fluoro-2-methoxypyridin-3-yl]methyl)-5-(5-methyl-1H-pyrrolo[2,3-b]pyridin-3- yl)methyl; PPP3/calcineurin: protein phosphatase 3; SBEs: STAT3 binding elements; shRNA: small hairpin RNA; SLC17A7/VGLUT1: solute carrier family 17 member 7; SLC32A1/VGAT: solute carrier family 32 member 1; STAT3: signal transducer and activator of transcription 3, TFEB: transcription factor EB; Ub: ubiquitin.

TFEB

Cav1.2

10.1080/15548627.2022.2162244

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Citations (15)