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Article ; Online: Neuron Derived Cold-Inducible RNA-Binding Protein Promotes NETs Formation to Exacerbate Brain Endothelial Barrier Disruption after Ischemic Stroke.

Li, Zhifang / Sun, Shuai / Xiao, Qinghui / Tan, Senwei / Jin, Huijuan / Hu, Bo

2024

Abstract: In ischemic stroke, neutrophils are the first-line peripheral immune cells infiltrating the brain tissue to form neutrophil extracellular traps (NETs). The present study aimed to investigate the role of neuronal cold-inducible RNA-binding protein (CIRP) ... ...

Abstract	In ischemic stroke, neutrophils are the first-line peripheral immune cells infiltrating the brain tissue to form neutrophil extracellular traps (NETs). The present study aimed to investigate the role of neuronal cold-inducible RNA-binding protein (CIRP) in promoting NETs-induced brain endothelial barrier destruction and cerebral edema after ischemic stroke. We found that the expression of NETs and neuronal CIRP in the penumbra increased at 6 hours after transient middle cerebral artery occlusion (tMCAO) and increased significantly at 24 hours, reaching a peak at 3 days. NETs degradation or CIRP inhibition can alleviate the leakage of brain endothelial barrier and reverse the decreased expression of tight junction proteins (zonula occludens-1, claudin-5 and occludin) in tMCAO mice. Oxygen-glucose deprivation/reperfusion treated primary neurons or recombinant CIRP could induce NETs formation via TLR4/p38 signaling pathway in vitro. Transcription factor specificity protein 1 (sp1) was responsible for the increased neuronal CIRP expression and the inhibition of sp1 could suppress the increased CIRP expression, reduce NETs formation, and diminish brain endothelial barrier leakage in tMCAO mice. We also found the upregulated CIRP level was associated with severe cerebral edema in patients with acute ischemic stroke. In conclusion, the increased expression of transcription factor sp1 after ischemic stroke can lead to elevated CIRP expression and release from the neurons, which subsequently interacts with neutrophils and promotes NETs formation, resulting in brain endothelial barrier destruction and cerebral edema.
Language	English
Publishing date	2024-02-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625789-0
ISSN	2152-5250 ; 2152-5250
ISSN (online)	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2024.0204-1
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Article ; Online: An updated review on prediction and preventive treatment of post-stroke depression.

Sun, Shuai / Li, Zhifang / Xiao, Qinghui / Tan, Senwei / Hu, Bo / Jin, Huijuan

Expert review of neurotherapeutics

2023 Volume 23, Issue 8, Page(s) 721–739

Abstract: Introduction: Post-stroke depression (PSD), one of the most common complications following stroke, affects approximately one-third of stroke patients and is significantly associated with increased disability and mortality as well as decreased quality of ...

Abstract	Introduction: Post-stroke depression (PSD), one of the most common complications following stroke, affects approximately one-third of stroke patients and is significantly associated with increased disability and mortality as well as decreased quality of life, which makes it an important public health concern. Treatment of PSD significantly ameliorates depressive symptoms and improves the prognosis of stroke. Areas covered: The authors discuss the critical aspects of the clinical application of prediction and preventive treatment of PSD. Then, the authors update the biological factors associated with the onset of PSD. Furthermore, they summarize the recent progress in pharmacological preventive treatment in clinical trials and propose potential treatment targets. The authors also discuss the current roadblocks in the preventive treatment of PSD. Finally, the authors put postulate potential directions for future studies so as to discover accurate predictors and provide individualized preventive treatment. Expert opinion: Sorting out high-risk PSD patients using reliable predictors will greatly assist PSD management. Indeed, some predictors not only predict the incidence of PSD but also predict prognosis, which indicates that they might also aid the development of an individualized treatment scheme. Preventive application of antidepressants may also be considered.
MeSH term(s)	Humans ; Depression/etiology ; Depression/prevention & control ; Quality of Life ; Risk Factors ; Stroke/drug therapy ; Antidepressive Agents/therapeutic use
Chemical Substances	Antidepressive Agents
Language	English
Publishing date	2023-07-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2112534-X
ISSN	1744-8360 ; 1473-7175
ISSN (online)	1744-8360
ISSN	1473-7175
DOI	10.1080/14737175.2023.2234081
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Zs.A 6155: Show issues

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Article ; Online: Extracellular vesicles: A new communication paradigm of complement in neurological diseases.

Gu, Xinmei / Chen, Anqi / Su, Ying / You, Mingfeng / Guo, Hongxiu / Tan, Senwei / He, Quanwei / Hu, Bo

Brain research bulletin

2023 Volume 199, Page(s) 110667

Abstract: The complement system is crucial to the innate immune system. It has the function of destroying pathogens by activating the classical, alternative, and lectin pathways. The complement system is important in nervous system diseases such as cerebrovascular ...

Abstract	The complement system is crucial to the innate immune system. It has the function of destroying pathogens by activating the classical, alternative, and lectin pathways. The complement system is important in nervous system diseases such as cerebrovascular and neurodegenerative diseases. Activation of the complement system involves a series of intercellular signaling and cascade reactions. However, research on the source and transport mechanisms of the complement system in neurological diseases is still in its infancy. Studies have increasingly found that extracellular vesicles (EVs), a classic intercellular communication paradigm, may play a role in complement signaling disorders. Here, we systematically review the EV-mediated activation of complement pathways in different neurological diseases. We also discuss the prospect of EVs as future immunotherapy targets.
MeSH term(s)	Humans ; Extracellular Vesicles/metabolism ; Complement System Proteins/metabolism ; Neurodegenerative Diseases/metabolism ; Cell Communication ; Signal Transduction
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2023-05-14
Publishing country	United States
Document type	Systematic Review ; Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	197620-5
ISSN	1873-2747 ; 0361-9230
ISSN (online)	1873-2747
ISSN	0361-9230
DOI	10.1016/j.brainresbull.2023.110667
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Zs.A 1243: Show issues

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Article: Genetics of Spontaneous Intracerebral Hemorrhage: Risk and Outcome.

Guo, Hongxiu / You, Mingfeng / Wu, Jiehong / Chen, Anqi / Wan, Yan / Gu, Xinmei / Tan, Senwei / Xu, Yating / He, Quanwei / Hu, Bo

Frontiers in neuroscience

2022 Volume 16, Page(s) 874962

Abstract: Spontaneous intracerebral hemorrhage (ICH) is a common fatal event without an effective therapy. Of note, some familial aggregation and inherited tendency is found in ICH and heritability estimates indicate that genetic variations contribute ... ...

Abstract	Spontaneous intracerebral hemorrhage (ICH) is a common fatal event without an effective therapy. Of note, some familial aggregation and inherited tendency is found in ICH and heritability estimates indicate that genetic variations contribute substantially to ICH risk and outcome. Thus, identification of genetic variants that affect the occurrence and outcome may be helpful for ICH prevention and therapy. There are several reviews summarizing numerous genetic variants associated with the occurrence of ICH before, but genetic variants contributing to location distribution and outcome have rarely been introduced. Here, we summarize the current knowledge of genetic variants and pay special attention to location distribution and outcome. So far, investigations have reveled variations in
Language	English
Publishing date	2022-04-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.874962
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Article ; Online: KCTD10 regulates brain development by destabilizing brain disorder-associated protein KCTD13.

Cheng, Jianbo / Wang, Zhen / Tang, Manpei / Zhang, Wen / Li, Guozhong / Tan, Senwei / Mu, Chenjun / Hu, Mengyuan / Zhang, Dan / Jia, Xiangbin / Wen, Yangxuan / Guo, Hui / Xu, Dan / Liu, Liang / Li, Jiada / Xia, Kun / Li, Faxiang / Duan, Ranhui / Xu, Zhiheng /

Yuan, Ling

Proceedings of the National Academy of Sciences of the United States of America

2024 Volume 121, Issue 12, Page(s) e2315707121

Abstract: KCTD10 belongs to the KCTD (potassiumchannel tetramerization domain) family, many members of which are associated with neuropsychiatric disorders. However, the biological function underlying the association with brain disorders remains to be explored. ... ...

Abstract	KCTD10 belongs to the KCTD (potassiumchannel tetramerization domain) family, many members of which are associated with neuropsychiatric disorders. However, the biological function underlying the association with brain disorders remains to be explored. Here, we reveal that Kctd10 is highly expressed in neuronal progenitors and layer V neurons throughout brain development.
MeSH term(s)	Animals ; Mice ; Proteins/metabolism ; Brain/metabolism ; Neurons/metabolism ; Neurodevelopmental Disorders/genetics ; Brain Diseases/genetics ; Neurogenesis/genetics ; Potassium Channels, Voltage-Gated/metabolism
Chemical Substances	Proteins ; KCTD10 protein, mouse ; Potassium Channels, Voltage-Gated
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2315707121
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Zs.A 1148: Show issues

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Article: Loss-of-function of KMT5B leads to neurodevelopmental disorder and impairs neuronal development and neurogenesis

Chen, Guodong / Han, Lin / Tan, Senwei / Jia, Xiangbin / Wu, Huidan / Quan, Yingting / Zhang, Qiumeng / Yu, Bin / Hu, Zhengmao / Xia, Kun / Guo, Hui

Journal of genetics and genomics. 2022 Mar. 06,

2022

Abstract: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders that cause severe social, communication and behavioral problems. Recent studies show that the variants of a histone methyltransferase gene KMT5B, cause neurodevelopmental disorders ...

Abstract	Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders that cause severe social, communication and behavioral problems. Recent studies show that the variants of a histone methyltransferase gene KMT5B, cause neurodevelopmental disorders (NDDs), including ASD and the knockout of Kmt5b in mice is embryonic lethal. However, the detailed genotype-phenotype correlations and functional effects of KMT5B in neurodevelopment are unclear. By targeted sequencing of a large Chinese ASD cohort, analyzing published genome-wide sequencing data, and mining literature, we curated 39 KMT5B variants identified from NDD individuals. A genotype-phenotype correlation analysis for ten individuals with KMT5B pathogenic variants reveals common symptoms, including ASD, intellectual disability, languages problem and macrocephaly. In vitro knockdown of the expression of Kmt5b in cultured mouse primary cortical neurons leads to a decrease in neuronal dendritic complexity and an increase in dendritic spine density, which can be rescued by expression of human KMT5B but not that of pathogenic de novo missense mutants. In vivo knockdown of the Kmt5b expression in the mouse embryonic cerebral cortex by in utero electroporation results in decreased proliferation and accelerated migration of neural progenitor cells. Our findings reveal essential roles of histone methyltransferase KMT5B in neuronal development, prenatal neurogenesis, and neuronal migration.
Keywords	autism ; cerebral cortex ; dendrites ; electroporation ; genes ; genomics ; genotype-phenotype correlation ; histones ; humans ; loss-of-function mutation ; methyltransferases ; mice ; neurodevelopment ; neurogenesis
Language	English
Dates of publication	2022-0306
Publishing place	Elsevier Ltd
Document type	Article
Note	Pre-press version
ZDB-ID	2374568-X
ISSN	1873-5533 ; 1673-8527
ISSN (online)	1873-5533
ISSN	1673-8527
DOI	10.1016/j.jgg.2022.03.004
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Targeted sequencing identifies risk variants in 202 candidate genes for neurodevelopmental disorders.

Pang, Nan / Li, Kuokuo / Tan, Senwei / Chen, Meilin / He, Fang / Chen, Chen / Yang, Lifen / Zhang, Ciliu / Deng, Xiaolu / Yang, Li / Mao, Leilei / Wang, Guoli / Duan, Haolin / Wang, Xiaole / Zhang, Wen / Guo, Hui / Peng, Jing / Yin, Fei / Xia, Kun

Gene

2023 Volume 897, Page(s) 148071

Abstract: With the continuous deepening of genetic research on neurodevelopmental disorders (NDDs), more patients have been identified the causal or candidate genes. However, it is still urgent needed to increase the sample size to confirm the associations between ...

Abstract	With the continuous deepening of genetic research on neurodevelopmental disorders (NDDs), more patients have been identified the causal or candidate genes. However, it is still urgent needed to increase the sample size to confirm the associations between variants and clinical manifestations. We previously performed molecular inversion probe sequencing of autism spectrum disorder (ASD) candidate genes in 1543 ASD patients. In this study, we used the same method to detect de novo variants (DNVs) in 665 NDD patients with intellectual disability (ID) and/or epilepsy (EP) for genetic analysis and diagnosis. We compared findings from ID/EP and ASD patients to improve our understanding of different subgroups of NDDs. We identified 72 novel variants and 39 DNVs. A totally of 5.71 % (38/665) of the patients were genetically diagnosed by this sequencing strategy. ID/EP patients demonstrated a higher prevalence of likely gene disruptive DNVs in ASD genes than the healthy population. Regarding high-risk genes, SCN1A and CKDL5 were more frequently mutated in ID/EP patients than in ASD patients. Our data provide an overview of the mutation burden in ID/EP patients from the perspective of high risk ASD genes, indicating the differences and association of NDDs subgroups.
MeSH term(s)	Humans ; Autism Spectrum Disorder/genetics ; Neurodevelopmental Disorders/genetics ; Intellectual Disability/genetics ; Epilepsy/genetics ; Genetic Predisposition to Disease
Language	English
Publishing date	2023-12-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2023.148071
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Zs.A 1357: Show issues

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Article ; Online: De novo variants in the PABP domain of PABPC1 lead to developmental delay.

Wegler, Meret / Jia, Xiangbin / Alders, Marielle / Bouman, Arjan / Chen, Jia / Duan, Xinyu / Lauzon, Julie L / Mathijssen, Inge B / Sticht, Heinrich / Syrbe, Steffen / Tan, Senwei / Guo, Hui / Abou Jamra, Rami

Genetics in medicine : official journal of the American College of Medical Genetics

2022 Volume 24, Issue 8, Page(s) 1761–1773

Abstract: Purpose: The study aimed to investigate the role of PABPC1 in developmental delay (DD).: Methods: Children were examined by geneticists and pediatricians. Variants were identified using exome sequencing and standard downstream bioinformatics ... ...

Abstract	Purpose: The study aimed to investigate the role of PABPC1 in developmental delay (DD). Methods: Children were examined by geneticists and pediatricians. Variants were identified using exome sequencing and standard downstream bioinformatics pipelines. We performed in silico molecular modeling and coimmunoprecipitation to test if the variants affect the interaction between PABPC1 and PAIP2. We performed in utero electroporation of mouse embryo brains to enlighten the function of PABPC1. Results: We describe 4 probands with an overlapping phenotype of DD, expressive speech delay, and autistic features and heterozygous de novo variants that cluster in the PABP domain of PABPC1. Further symptoms were seizures and behavioral disorders. Molecular modeling predicted that the variants are pathogenic and would lead to decreased binding affinity to messenger RNA metabolism-related proteins, such as PAIP2. Coimmunoprecipitation confirmed this because it showed a significant weakening of the interaction between mutant PABPC1 and PAIP2. Electroporation of mouse embryo brains showed that Pabpc1 knockdown decreases the proliferation of neural progenitor cells. Wild-type Pabpc1 could rescue this disturbance, whereas 3 of the 4 variants did not. Conclusion: Pathogenic variants in the PABP domain lead to DD, possibly because of interference with the translation initiation and subsequently an impaired neurogenesis in cortical development.
MeSH term(s)	Animals ; Child ; Developmental Disabilities/genetics ; Heterozygote ; Humans ; Intellectual Disability/genetics ; Mice ; Neurodevelopmental Disorders/genetics ; Poly(A)-Binding Protein I/chemistry ; Poly(A)-Binding Protein I/metabolism ; RNA, Messenger ; RNA-Binding Proteins/genetics ; Whole Exome Sequencing
Chemical Substances	Poly(A)-Binding Protein I ; RNA, Messenger ; RNA-Binding Proteins
Language	English
Publishing date	2022-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1016/j.gim.2022.04.013
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Zs.A 5059: Show issues

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Article: Loss-of-function of KMT5B leads to neurodevelopmental disorder and impairs neuronal development and neurogenesis.

Chen, Guodong / Han, Lin / Tan, Senwei / Jia, Xiangbin / Wu, Huidan / Quan, Yingting / Zhang, Qiumeng / Yu, Bin / Hu, Zhengmao / Xia, Kun / Guo, Hui

Journal of genetics and genomics = Yi chuan xue bao

2022 Volume 49, Issue 9, Page(s) 881–890

Abstract: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders that cause severe social, communication, and behavioral problems. Recent studies show that the variants of a histone methyltransferase gene KMT5B cause neurodevelopmental disorders ...

Abstract	Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders that cause severe social, communication, and behavioral problems. Recent studies show that the variants of a histone methyltransferase gene KMT5B cause neurodevelopmental disorders (NDDs), including ASD, and the knockout of Kmt5b in mice is embryonic lethal. However, the detailed genotype-phenotype correlations and functional effects of KMT5B in neurodevelopment are unclear. By targeted sequencing of a large Chinese ASD cohort, analyzing published genome-wide sequencing data, and mining literature, we curated 39 KMT5B variants identified from NDD individuals. A genotype-phenotype correlation analysis for 10 individuals with KMT5B pathogenic variants reveals common symptoms, including ASD, intellectual disability, languages problem, and macrocephaly. In vitro knockdown of the expression of Kmt5b in cultured mouse primary cortical neurons leads to a decrease in neuronal dendritic complexity and an increase in dendritic spine density, which can be rescued by expression of human KMT5B but not that of pathogenic de novo missense mutants. In vivo knockdown of the Kmt5b expression in the mouse embryonic cerebral cortex by in utero electroporation results in decreased proliferation and accelerated migration of neural progenitor cells. Our findings reveal essential roles of histone methyltransferase KMT5B in neuronal development, prenatal neurogenesis, and neuronal migration.
MeSH term(s)	Animals ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/pathology ; Female ; Histone Methyltransferases ; Humans ; Intellectual Disability/genetics ; Mice ; Neurodevelopmental Disorders/genetics ; Neurogenesis/genetics ; Pregnancy
Chemical Substances	Histone Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2022-03-21
Publishing country	China
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2374568-X
ISSN	1873-5533 ; 1673-8527
ISSN (online)	1873-5533
ISSN	1673-8527
DOI	10.1016/j.jgg.2022.03.004
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Article ; Online: Effects of Different Substrates on Lignocellulosic Enzyme Expression, Enzyme Activity, Substrate Utilization and Biological Efficiency of Pleurotus Eryngii.

Xie, Chunliang / Yan, Li / Gong, Wenbing / Zhu, Zuohua / Tan, Senwei / Chen, Du / Hu, Zhenxiu / Peng, Yuande

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2016 Volume 39, Issue 4, Page(s) 1479–1494

Abstract: Background/aims: Pleurotus eryngii is one of the most valued and delicious mushrooms which are commercially cultivated on various agro-wastes. How different substrates affect lignocellulosic biomass degradation, lignocellulosic enzyme production and ... ...

Abstract	Background/aims: Pleurotus eryngii is one of the most valued and delicious mushrooms which are commercially cultivated on various agro-wastes. How different substrates affect lignocellulosic biomass degradation, lignocellulosic enzyme production and biological efficiency in Pleurotus eryngii was unclear. Methods and results: In this report, Pleurotus eryngii was cultivated in substrates including ramie stalks, kenaf stalks, cottonseed hulls and bulrush stalks. The results showed that ramie stalks and kenaf stalks were found to best suitable to cultivate Pleurotus eryngii with the biological efficiency achieved at 55% and 57%, respectively. In order to establish correlations between different substrates and lignocellulosic enzymes expression, the extracellular proteins from four substrates were profiled with high throughput TMT-based quantitative proteomic approach. 241 non-redundant proteins were identified and 74 high confidence lignocellulosic enzymes were quantified. Most of the cellulases, hemicellulases and lignin depolymerization enzymes were highly up-regulated when ramie stalks and kenaf stalks were used as carbon sources. The enzyme activities results suggested cellulases, hemicellulases and lignin depolymerization enzymes were significantly induced by ramie stalks and kenaf stalks. Conclusion: The lignocelluloses degradation, most of the lignocellulosic enzymes expressions and activities of Pleurotus eryngii had positive correlation with the biological efficiency, which depend on the nature of lignocellulosic substrates. In addition, the lignocellulosic enzymes expression profiles during Pleurotus eryngii growth in different substrates were obtained. The present study suggested that most of the lignocellulosic enzymes expressions and activities can be used as tools for selecting better performing substrates for commercial mushroom cultivation.
MeSH term(s)	Biomass ; Cellulases/genetics ; Cellulases/isolation & purification ; Cellulases/metabolism ; Crops, Agricultural ; Enzyme Assays ; Fungal Proteins/genetics ; Fungal Proteins/isolation & purification ; Fungal Proteins/metabolism ; Gene Expression ; Glycoside Hydrolases/genetics ; Glycoside Hydrolases/isolation & purification ; Glycoside Hydrolases/metabolism ; Hydrolysis ; Lignin/chemistry ; Lignin/metabolism ; Molecular Sequence Annotation ; Pleurotus/enzymology ; Pleurotus/genetics ; Proteomics/methods ; Substrate Specificity ; Waste Products
Chemical Substances	Fungal Proteins ; Waste Products ; lignocellulose (11132-73-3) ; Lignin (9005-53-2) ; Cellulases (EC 3.2.1.-) ; Glycoside Hydrolases (EC 3.2.1.-) ; hemicellulase (EC 3.2.1.-)
Language	English
Publishing date	2016-09-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000447851
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