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HSP110 aggravates ischemia-reperfusion injury after liver transplantation by promoting NF-κB pathway

Hepatobiliary & Pancreatic Diseases International 2024年第4期23卷 344-352页

作者： Qing-Zhi Hu Zhen-Rui Cao Wei-Xiong Zheng Min-Jie Zhao Jun-Hua Gong Cong Chen Zhong-Jun Wu Rui Tao Department of Hepatobiliary Surgery Bishan Hospital of Chongqing Medical UniversityChongqing 402760China Department of Cardiothoracic Surgery the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China c Department of Hepatobiliary Surgery the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Department of Hepatobiliary Surgery the Second Affiliated Hospital of Chongqing Medical UniversityChongqing 400010China

Background:Ischemia-reperfusion injury(IRI)poses a significant challenge to liver transplantation(LT).The underlying mechanism primarily involves overactivation of the immune *** shock protein 110(HSP110)functions as a molecular chaperone that helps stabilize protein ***:An IRI model was established by performing LT on Sprague-Dawley rats,and HSP110 was silenced using ***-eosin staining,TUNEL,immunohistochemistry,ELISA and liver enzyme analysis were performed to assess IRI following *** blotting and quantitative reverse transcription-polymerase chain reaction were conducted to investigate the pertinent molecular ***:Our findings revealed a significant increase in the expression of HSP110 at both the mRNA and protein levels in the rat liver following LT(P<0.05).However,when rats were injected with siRNAHSP110,IRI subsequent to LT was notably reduced(P<0.05).Additionally,the levels of liver enzymes and inflammatory chemokines in rat serum were significantly reduced(P<0.05).Silencing HSP110 with siRNA resulted in a marked decrease in M1-type polarization of Kupffer cells in the liver and downregulated the NF-κB pathway in the liver(P<0.05).Conclusions:HSP110 in the liver promotes IRI after LT in rats by activating the NF-κB pathway and inducing M1-type polarization of Kupffer *** HSP110 to prevent IRI after LT may represent a promising new approach for the treatment of LT-associated IRI.

关键词： Ischemia-reperfusion injury Liver transplantation Inflammation HSP110 Heat shock proteins NF-κB

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Revolutionizing tumor immunotherapy:unleashing the power of progenitor exhausted T cells

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Cancer Biology & Medicine 2024年第6期21卷 499-512页

作者： Zhang Fang Xinyi Ding Hao Huang Hongwei Jiang Jingting Jiang Xiao Zheng Department of Tumor Biological Treatment The Third Affiliated Hospital of Soochow UniversityChangzhou 213003China Jiangsu Engineering Research Center for Tumor Immunotherapy The Third Affiliated Hospital of Soochow UniversityChangzhou 213003China Institute for Cell Therapy of Soochow university The Third Affiliated Hospital of Soochow UniversityChangzhou 213003China

In exploring persistent infections and malignancies, a distinctive subgroup of CD8^(+) T cells, progenitor exhausted CD8^(+) T(Tpex) cells, has been identified. These Tpex cells are notable for their remarkable self-renewal and rapid proliferation abilities. Recent strides in immunotherapy have demonstrated that Tpex cells expand and differentiate into responsive exhausted CD8^(+) T cells, thus underscoring their critical role in the immunotherapeutic retort. Clinical examinations have further clarified a robust positive correlation between the proportional abundance of Tpex cells and enhanced clinical prognosis. Tpex cells have found noteworthy applications in the formulation of inventive immunotherapeutic approaches against tumors. This review describes the functions of Tpex cells in the tumor milieu, particularly their potential utility in tumor immunotherapy. Precisely directing Tpex cells may be essential to achieving successful outcomes in immunotherapy against tumors.

关键词： Progenitor exhausted CD8^(+)T cells TCF-1 immunotherapy tumor microenvironment cellular crosstalk

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MPZL1 as an HGF/MET signaling amplifier promotes cell migration and invasion in glioblastoma

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Genes & Diseases 2024年第5期11卷 70-73页

作者： Haimin Song Bowen Ni Xuetao Peng Weijuan Xu Shaochun Yang Runwei Yang Ziyu Wang Kaishu Li Rui Lin Yunxiao Zhang Jinglin Guo Kezhi Wu Guangwei Shi Jichao Sun Chunming He Yawei Liu Department of Neurosurgery The First Affiliated Hospital of Gannan Medical UniversityGanzhouJiangxi 341000China Department of Neurosurgery&Medical Research Center Shunde HospitalSouthern Medical University(The First People’s Hospital of Shunde Foshan)FoshanGuangdong 528300China Medical Research Center Shunde HospitalSouthern Medical University(The First People’s Hospital of Shunde Foshan)FoshanGuangdong 528300China Bidding and Procurement Office Shunde HospitalSouthern Medical University(The First People’s Hospital of Shunde Foshan)FoshanGuangdong 528300China Department of Neurosurgery Nanfang HospitalSouthern Medical UniversityGuangzhouGuangdong 510515China Department of Neurosurgery The Sixth Affiliated Hospital of Guangzhou Medical UniversityQingyuanGuangdong 511518China Department of Neurosurgery The First Affiliated Hospital of Shantou University Medical CollegeShantouGuangdong 515041China Department of Geriatrics Shenzhen People’s Hospital(The Second Clinical Medical CollegeJinan UniversityThe First Affiliated HospitalSouthern University of Science and Technology)ShenzhenGuangdong 518020China

The extremely poor prognosis of patients is largely due to hepatocyte growth factor(HGF)/MET signaling,which promotes migration and invasion of glioblastoma(IDH wildtype;GBM;WHO grade 4).1,2 Clinical trials targeting MET,the only receptor of HGF,have yielded unimpressive results in GBM.3,4 Here we found that HGF induced strong chemotaxis on GBM cells,but MET expression was extremely ***,therefore,used single-cell RNA sequencing(scRNA-seq)coupled with label-free proteome profiling to identify membrane proteins associated with HGF/MET signaling amplification in GBM and to provide a novel modulator,MPZL1,for HGF/MET-targeted therapy.

关键词： invasion prognosis Clinical

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Intermittent Theta Burst Stimulation Attenuates Cognitive Deficits and Alzheimer’s Disease-Type Pathologies via ISCA1-Mediated Mitochondrial Modulation in APP/PS1 Mice

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Neuroscience Bulletin 2024年第2期40卷 182-200页

作者： Yang Zhu Hao Huang Zhi Chen Yong Tao Ling-Yi Liao Shi-Hao Gao Yan-Jiang Wang Chang-Yue Gao Department of Rehabilitation Medicine Daping HospitalArmy Medical UniversityChongqing 400042China Department of Neurology and Center for Clinical Neuroscience Daping HospitalArmy Medical UniversityChongqing 400042China Department of Special Medicine Daping HospitalArmy Medical UniversityChongqing 400042China

Intermittent theta burst stimulation(iTBS),a time-saving and cost-effective repetitive transcranial magnetic stimulation regime,has been shown to improve cognition in patients with Alzheimer’s disease(AD).However,the specific mechanism underlying iTBS-induced cognitive enhancement remains *** studies suggested that mitochondrial functions are modulated by magnetic ***,we showed that iTBS upregulates the expression of iron-sulfur cluster assembly 1(ISCA1,an essential regulatory factor for mitochondrial respiration)in the brain of APP/PS1 *** vivo and in vitro studies revealed that iTBS modulates mitochondrial iron-sulfur cluster assembly to facilitate mitochondrial respiration and function,which is required for ***,iTBS rescues cognitive decline and attenuates AD-type pathologies in APP/PS1 *** present study uncovers a novel mechanism by which iTBS modulates mitochondrial respiration and function via ISCA1-mediated iron-sulfur cluster assembly to alleviate cognitive impairments and pathologies in *** provide the mechanistic target of iTBS that warrants its therapeutic potential for AD patients.

关键词： Intermittent theta burst stimulation Alzheimer’s disease Iron-sulfur cluster assembly 1 Mitochondrial dysfunction Neurodegeneration

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Suppression of mature TAU isoforms prevents Alzheimer's disease-like amyloid-beta oligomer-induced spine loss in rodent neurons

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Neural Regeneration Research 2024年第8期19卷 1655-1657页

作者： Sarah Buchholz Hans Zempel Institute of Human Genetics Faculty of Medicine and University Hospital CologneUniversity of CologneCologneGermany Center for Molecular Medicine Cologne(CMMC) Faculty of Medicine and University Hospital CologneUniversity of CologneCologneGermany

Introduction:TAU isoforms as disease mediators:The microtubule-associated protein TAU is predominantly present in the axons of neurons under physiological *** Alzheimer’s disease(AD)and related tauopathies,TAU also mislocalizes("TAU missorting")to the soma and the dendrites,where it eventually forms aggregates,the so-called neurofibrillary tangles(for review see Zimmer-Bensch and Zempel,2021;Zempel,2023).

关键词： Alzheimer Zimmer tau

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High-throughput sequencing analysis of differential microRNA expression in the process of blocking the progression of chronic atrophic gastritis to gastric cancer by Xianglian Huazhuo formula(香连化浊方)

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Journal of Traditional Chinese Medicine 2024年第4期44卷 703-712页

作者： GUO Yuxi LI Ze CHENG Nan JIA Xuemei WANG Jie MA Hongyu ZHAO Runyuan LI Bolin XUE Yucong CAI Yanru YANG Qian Department of spleen and stomach diseases First Affiliated Hospital of Hebei University of Traditional Chinese Medicine Department of Traditional Chinese Medicine Hebei General Hospital Department of Gastroenterology the First Affiliated Hospital of Guangzhou University of Chinese Medicine College of Integrative Medicine Hebei University of Chinese Medicine

OBJECTIVE: To explore the mechanism of Xianglian Huazhuo formula( 香连化浊方, XLHZ) blocking the development of chronic atrophic gastritis(CAG) to gastric cancer(GC) through bioinformatics analysis and in vitro. METHODS: Pathological morphology of gastric mucosa of rats were observed. High-throughput sequencing was used to analyze the miRNA expression profile of gastric mucosa. The miRanda, miRDB and miRWalk databases were used to predict the differential target genes. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis were performed for differential target genes. Real-time quantitative reverse transcription polymerase chain reaction(qRTPCR) was used to verify the differentially expressed miRNAs and target genes. Western blot, EdU, wound healing and flow cytometry were used to observe the effect of XLHZ on epithelial-mesenchymal transition(EMT) markers, proliferation, migration, apoptosis and cell cycle of CAG cells in vitro. RESULTS: A total of five differentially expressed miRNAs and four differential target genes were screened in this study. GO analysis showed that the target genes were enriched in regulation of neuron development, regulation of transcription factor activity and regulation of RNA polymerase. KEGG pathways database differences in gene enrichment of target genes in the Wnt signaling pathway, Phospholipase D signaling pathway and mitogen-activated protein kinase signaling pathway. qRTPCR confirmed that miRNAs and its target genes were consistent with the screening results. In vitro, our study revealed that XLHZ could increase the expression of Ecadherin, decrease the expression of transforming growth factor β1, vimentin and β-catenin, inhibite the proliferation and migration of CAG cells, cause cell cycle arrest at G0/G1 and G2/M phase, induce the apoptosis of CAG cells, and prevent the progression of CAG to GC. CONCLUSION: This study provided a new idea for the mechanism of blocking the progression of CAG to GC b

关键词： Xianglian Huazhuo formula gastritis, atrophic high-throughput nucleotide sequencing microRNAs stomach neoplasms

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NOX4 promotes tumor progression through the MAPK-MEK1/2-ERK1/2 axis in colorectal cancer

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World Journal of Gastrointestinal Oncology 2024年第4期16卷 1421-1436页

作者： Yu-Jie Xu Ya-Chang Huo Qi-Tai Zhao Jin-Yan Liu Yi-Jun Tian Lei-Lei Yang Yi Zhang Biotherapy Center and Cancer Center The First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052Henan ProvinceChina Department of Oncology Henan Provincial People’s HospitalPeople’s Hospital of Zhengzhou UniversityPeople’s Hospital of Henan UniversityZhengzhou 450003Henan ProvinceChina

BACKGROUND Metabolic reprogramming plays a key role in cancer progression and clinical outcomes;however,the patterns and primary regulators of metabolic reprogramming in colorectal cancer(CRC)are not well *** To explore the role of nicotinamide adenine dinucleotide phosphate oxidase 4(NOX4)in promoting progression of *** We evaluated the expression and function of dysregulated and survival-related metabolic genes using Gene Ontology and Kyoto Encyclopedia of Genes and *** clustering was used to cluster CRC based on dysregulated metabolic genes.A prediction model was constructed based on survival-related metabolic *** formation,migration,invasion,proliferation,apoptosis and clone formation was used to evaluate the biological function of NOX4 in *** sequencing was utilized to explore the alterations of gene expression NOX4 over-expression tumor *** vivo subcutaneous and lung metastasis mouse tumor model was used to explore the effect of NOX4 on tumor *** We comprehensively analyzed 3341 metabolic genes in CRC and identified three clusters based on dysregulated metabolic *** these genes,NOX4 was highly expressed in tumor tissues and correlated with worse *** vitro,NOX4 overexpression induced clone formation,migration,invasion,and stemness in CRC ***,RNA-sequencing analysis revealed that NOX4 overexpression activated the mitogen-activated protein kinase-MEK1/2-ERK1/2 signaling ***,a MEK1/2 inhibitor,abolished the NOX4-mediated tumor *** vivo,NOX4 overexpression promoted subcutaneous tumor growth and lung metastasis,whereas trametinib treatment can reversed the *** Our study comprehensively analyzed metabolic gene expression and highlighted the importance of NOX4 in promoting CRC metastasis,suggesting that trametinib could be a potential therapeutic drugs of CRC clinical therapy targeting NOX4.

关键词： Colorectal cancer Metabolic reprogramming Metastasis Nicotinamide adenine dinucleotide phosphate oxidase 4 Mitogen-activated protein kinase signaling

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Biomarkers for neuromyelitis optica:a visual analysis of emerging research trends

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Neural Regeneration Research 2024年第12期19卷 2735-2749页

作者： Xiangjun Li Jiandong Zhang Siqi Zhang Shengling Shi Yi’an Lu Ying Leng Chunyan Li Department of Ophthalmology Affiliated Hospital of Beihua UniversityJilinJilin ProvinceChina Department of Ophthalmology Changchun Bright Eye HospitalChangchunJilin ProvinceChina Departemt of Endocrinology Affiliated Hospital of Beihua UniversityJilinJilin ProvinceChina

Neuromyelitis optica is an inflammatory demyelinating disease of the central nervous system that differs from multiple *** the past 20 years,the search for biomarke rs for neuromyelitis optica has been ***,we used a bibliometric approach to analyze the main research focus in the field of biomarkers for neuromyelitis *** in this area is consistently increasing,with China and the United States leading the way on the number of studies *** Mayo Clinic is a highly reputable institution in the United States,and was identified as the most authoritative institution in this ***,Professor Wingerchuk from the Mayo Clinic was the most authoritative expe rt in this *** analysis revealed that the terms "neuro myelitis optica"(261 times), "multiple sclerosis"(220 times), "neuromyelitis optica spectrum disorder"(132 times), "aquaporin4"(99 times),and "optical neuritis"(87 times) were the most frequently used keywords in literature related to this *** analysis of the classical literature showed that the majority of publications provide conclusive research evidence supporting the use of aquaporin-4-IgG and neuromyelitis optica-IgG to effectively diagnose and differentiate neuromyelitis optica from multiple ***,aquaporin-4-IgG has emerged as a highly specific diagnostic biomarker for neuromyelitis optica spectrum *** oligodendrocyte glycoprotein-IgG is a diagnostic biomarke r for myelin oligodendrocyte glycoprotein antibody-associated *** biomarkers for neuromyelitis optica in clude cerebrospinal fluid immunological biomarkers such as glial fibrillary acidic protein,serum astrocyte damage biomarkers like FAM19A5,serum albumin,and gammaaminobutyric *** latest prospective clinical trials are exploring the potential of these *** results indicate that glial fibrillary acidic protein is emerging as a promising candidate biomarker for neuromyelit

关键词： aquaporin-4 autoantibody multiple sclerosis myelin oligodendrocyte glycoprotein antibody-associated disease neuromyelitis optica neuromyelitis optica spectrum disorder optical coherence tomography

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Single-Cell Mapping of Brain Myeloid Cell Subsets Reveals Key Transcriptomic Changes Favoring Neuroplasticity after Ischemic Stroke

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Neuroscience Bulletin 2024年第1期40卷 65-78页

作者： Fangxi Liu Xi Cheng Chuansheng Zhao Xiaoqian Zhang Chang Liu Shanshan Zhong Zhouyang Liu Xinyu Lin Wei Qiu Xiuchun Zhang Department of Neurology.The First Affiliated hospital of China Medical university Shenyang 110001China Department of Neurology The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510630China Stroke Center The First Affiliated Hospital of China Medical UniversityShenyang 110001China

Interactions between brain-resident and periph-eral infiltrated immune cells are thought to contribute to neuroplasticity after cerebral ***,con-ventional bulk sequencing makes it challenging to depict this complex immune *** single-cell RNA sequencing,we mapped compositional and transcriptional features of peri-infarct immune *** were the predominant cell type in the peri-infarct region,displaying a more diverse activation pattern than the typical pro-and anti-inflammatory state,with axon tract-associated micro-glia(ATMs)being associated with neuronal *** inference suggested that infiltrated monocyte-derived macrophages(MDMs)exhibited a gradual fate trajectory transition to activated ***-cellular crosstalk between MDMs and microglia orchestrated anti-inflammatory and repair-promoting microglia phenotypes and promoted post-stroke neurogenesis,with SOX2 and related Akt/CREB signaling as the underlying *** description of the brain's immune landscape and its relationship with neurogenesis provides new insight into promoting neural repair by regulating neuroinflammatory responses.

关键词： Ischemic stroke Monocyte-derived macrophage Microglia Neurogenesis Single-cell sequencing

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GNAS mutations suppress cell invasion by activating MEG3 in growth hormone–secreting pituitary adenoma

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Oncology Research 2024年第6期32卷 1079-1091页

作者： CHAO TANG CHUNYU ZHONG JUNHAO ZHU FENG YUAN JIN YANG YONG XU CHIYUAN MA Department of Neurosurgery Affiliated Jinling HospitalMedical School of Nanjing UniversityNanjing210002China Department of Neurosurgery Children’s Hospital of Nanjing Medical UniversityNanjing210019China Affiliated Eye hospital Nanjing Medical UniversityNanjing210029China Department of Neurosurgery Jinling HospitalSouthern Medical UniversityNanjing210002China Department of Neurosurgery Jinling HospitalNanjing Medical UniversityNanjing210002China

Approximately 30%–40%of growth hormone–secreting pituitary adenomas(GHPAs)harbor somatic activating mutations in GNAS(αsubunit of stimulatory G protein).Mutations in GNAS are associated with clinical features of smaller and less invasive ***,the role of GNAS mutations in the invasiveness of GHPAs is *** mutations were detected in GHPAs using a standard polymerase chain reaction(PCR)sequencing *** expression of mutation-associated maternally expressed gene 3(MEG3)was evaluated with ***3 was manipulated in GH3 cells using a lentiviral expression *** invasion ability was measured using a Transwell assay,and epithelial–mesenchymal transition(EMT)-associated proteins were quantified by immunofluorescence and western ***,a tumor cell xenograft mouse model was used to verify the effect of MEG3 on tumor growth and *** invasiveness of GHPAs was significantly decreased in mice with mutated GNAS compared with that in mice with wild-type ***,the invasiveness of mutant GNASexpressing GH3 cells ***3 is uniquely expressed at high levels in GHPAs harboring mutated ***,MEG3 upregulation inhibited tumor cell invasion,and conversely,MEG3 downregulation increased tumor cell ***,GNAS mutations inhibit EMT in ***3 in mutated GNAS cells prevented cell invasion through the inactivation of the Wnt/β-catenin signaling pathway,which was further validated in *** data suggest that GNAS mutations may suppress cell invasion in GHPAs by regulating EMT through the activation of the MEG3/Wnt/β-catenin signaling pathway.

关键词： GHPAs GNAS mutation MEG3 β-catenin EMT

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