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H2S protects against diabetes-accelerated atherosclerosis by preventing the activation of NLRP3 inflammasome

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The Journal of Biomedical Research 2020年第2期34卷 94-102页

作者： Qiao Zheng Lihong Pan Yong Ji key laboratory of cardiovascular and cerebrovascular medicine Key Laboratory of Targeted Intervention of Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjingJiangsu 211166China

Hydrogen sulfide(H2S) is an important messenger for its strong anti-inflammatory effects, which may be involved in multiple cardiovascular diseases. In our previous study, we revealed that H2S attenuated diabetesaccelerated atherosclerosis through suppressing oxidative stress. Here we report that GYY4137, a H2S donor,reduced the plaque formation of aortic roots and the levels of both intercellular cell adhesion molecule 1(ICAM1)and vascular cell adhesion molecule 1(VCAM1) in diabetes-accelerated atherosclerotic cells and mouse *** inflammatory factors of TNF-α, IL-1β, IL-6, and MCP1 were also significantly reduced by ***, GYY4137 suppressed the activation of pyrin domain containing protein 3(NLRP3) inflammasome in diabetes-accelerated atherosclerosis conditions. Upon knockdown of NLRP3, the increase of ICAM1 and VCAM1 caused by high glucose and ox LDL could be reversed, indicating that H2S protected the endothelium by inhibiting the activity of NLRP3 inflammasome. In conclusion, our study indicates that GYY4137 effectively protects against the development of diabetes-accelerated atherosclerosis by inhibiting inflammasome activation.

关键词： H2S NLRP3 inflammation diabetes-accelerated atherosclerosis

γ-catenin alleviates cardiac fibrosis through inhibiting phosphorylation of GSK-3β

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The Journal of Biomedical Research 2020年第1期34卷 27-35页

作者： Xin Tang Jiaxin Tian Liping Xie Yong Ji key laboratory of cardiovascular and cerebrovascular medicine Key Laboratory of Targeted Intervention and Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjingJiangsu 211166China

Cardiac fibrosis is a common pathological change of many cardiovascular diseases. β-catenin has been shown to promote fibrosis. However, the precise role of its homolog γ-catenin in the process of fibrosis remains largely unclear. In this study, we found that the expression of γ-catenin was significantly decreased in angiotensin Ⅱ(Ang Ⅱ)-induced cardiac fibrosis model, contrary to most reports of β-catenin. Overexpression of γ-catenin in cardiac fibroblasts(CFs) significantly inhibited the expression of α-smooth muscle actin(α-SMA), whereas knocking down the expression of γ-catenin with si RNA promoted the occurrence of cardiac ***, γ-catenin could bind to GSK-3β to inhibit the phosphorylation of GSK-3β, therefore preventing cardiac fibrosis. Our study shows that γ-catenin is an important protective factor in cardiac fibrosis, which provides a new potential target for the treatment of cardiac fibrosis.

关键词： γ-catenin cardiac fibrosis GSK-3β

Significant implications of Bcl-2 in the formation of striatonigral projection neurons in the ischemic striatum

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Neuroscience Bulletin 2012年第6期28卷 667-668页

作者： Dong-Ya Zhu laboratory of cerebrovascular Disease Key Laboratory of Cardiovascular Disease and Molecular InterventionNanjing Medical University

In adult mammals, including humans, the subventricular zone （SVZ） of the lateral ventricles and the subgranular zone of the dentate gyms （DG） show ongoing neurogenesis. Cerebral ischemic insults trigger neurogenesis from neural stem cells or progenitor cells located in the SVZ and DG. Newborn neurons are then functionally recruited into the circuitry of the CA1 region, striatum and DG granule cell layer.

关键词： In Pro Significant implications of Bcl-2 in the formation of striatonigral projection neurons in the ischemic striatum SVZ

Orexin receptor type 2 agonism inhibits thermogenesis in brown adipose tissue by attenuating afferent innervation

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The Journal of Biomedical Research 2022年第3期36卷 195-207,I0005,I0006页

作者： Mo-qiu Jia Yong-jin Wang Kang Fu Han Jiao Jia Sun Yuanqing Gao key laboratory of cardiovascular and cerebrovascular medicine School of PharmacyNanjing Medical UniversityNanjingJiangsu 211166China

Orexin signaling has been associated with energy expenditure and brown adipose tissue(BAT)***,conflicting data exist in the field about how orexin signaling regulates BAT *** this study,we show that a specific orexin receptor type 2(OX2R)agonist[Ala11,D-Leu15]-OxB(OB-Ala)inhibited intrascapular brown adipose tissue(iBAT)thermogenesis by reducing sympathetic output to *** effect is mediated by OX2Rs located on afferent nerve endings innervating iBAT instead of brown adipocyte *** of OB-Ala into iBAT inhibited iBAT thermogenesis in mice upon cold exposure and neuronal activity in the paraventricular *** suggest that OB-Ala could inhibit iBAT thermogenesis by attenuating sensory input thereby inhibiting the sympathetic-sensory iBAT feedback *** study uncovers a novel primary action site of orexin in the regulation of energy balance.

关键词： orexin receptor type 2 brown adipose tissue thermogenesis

ImSpiRE: image feature-aided spatial resolution enhancement method

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Science China Life Sciences 2025年第1期 272-283页

作者： Yuwei Hua Yizhi Zhang Zhenming Guo Shan Bian Yong Zhang State key laboratory of cardiovascular Diseases and Medical Innovation Center Institute for Regenerative MedicineDepartment of NeurosurgeryShanghai East HospitalShanghai Key Laboratory of Signaling and Disease ResearchFrontier Science Center for Stem Cell ResearchSchool of Life Sciences and TechnologyTongji University

The resolution of most spatially resolved transcriptomic technologies usually cannot attain the single-cell level, limiting their applications in biological discoveries. Here, we introduce ImSpiRE, an image feature-aided spatial resolution enhancement method for in situ capturing spatial transcriptome. Taking the information stored in histological images, ImSpiRE solves an optimal transport problem to redistribute the expression profiles of spots to construct new transcriptional profiles with enhanced resolution, together with extending the gene expression profiles into unmeasured regions. Applications to multiple datasets confirm that ImSpiRE can enhance spatial resolution to the subspot level while contributing to the discovery of tissue domains, signaling communication patterns, and spatiotemporal characterization.

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ASF1A-dependent P300-mediated histone H3 lysine 18 lactylation promotes atherosclerosis by regulating EndMT

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Acta Pharmaceutica Sinica B 2024年第7期14卷 3027-3048页

作者： Mengdie Dong Yunjia Zhang Minghong Chen Yongkang Tan Jiao Min Xian He Fuhao Liu Jiaming Gu Hong Jiang Longbin Zheng Jiajing Chen Quanwen Yin Xuesong Li Xiang Chen Yongfeng Shao Yong Ji Hongshan Chen Department of cardiovascular Surgery the First Affiliated Hospital of Nanjing Medical Universityand Key Laboratory of Cardiovascular and Cerebrovascular MedicineSchool of PharmacyNational Vaccine Innovation PlatformNanjing Medical UniversityNanjing 211166China key laboratory of cardiovascular and cerebrovascular medicine School of PharmacyNanjing Medical UniversityNanjing 211166China Department of Clinical medicine Nanjing Medical University TIANYUAN Honors SchoolNanjing Medical UniversityNanjing 211166China Department of Anesthesiology Sir Run Run HospitalNanjing Medical UniversityNanjing 211166China Department of cardiovascular Surgery the First Affiliated Hospital of Nanjing Medical UniversityNanjing 211166China key laboratory of cardiovascular and cerebrovascular medicine Key Laboratory of Targeted Intervention of Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineState Key Laboratory of Reproductive MedicineSchool of Pharmacythe Affiliated Suzhou Hospital of Nanjing Medical UniversityGusu SchoolNanjing Medical UniversityNanjing 211166China National key laboratory of Frigid Zone cardiovascular Diseases(NKLFZCD) Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China)College of PharmacyKey Laboratory of Cardiovascular Medicine Research and Key Laboratory of Myocardial IschemiaChinese Ministry of EducationNHC Key Laboratory of Cell Transplantationthe Central Laboratory of the First Affiliated HospitalHarbin Medical UniversityHarbin 150081China key laboratory of Targeted Intervention of cardiovascular Disease Collaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjing 211166China Department of Cardiology Huai’an First People’s Hospital Affiliated with Nanjing Medical UniversityHuai’an 223399China

Endothelial-to-mesenchymal transition(EndMT)is a key driver of *** glycolysis is increased in the endothelium of atheroprone areas,accompanied by elevated lactate *** lactylation,mediated by lactate,can regulate gene expression and participate in disease ***,whether histone lactylation is involved in atherosclerosis remains ***,we report that lipid peroxidation could lead to EndMT-induced atherosclerosis by increasing lactatedependent histone H3 lysine 18 lactylation(H3K18la)in vitro and in vivo,as well as in atherosclerotic patients’***,the histone chaperone ASF1A was first identified as a cofactor of P300,which precisely regulated the enrichment of H3K18la at the promoter of SNAI1,thereby activating SNAI1 transcription and promoting *** found that deletion of ASF1A inhibited EndMT and improved endothelial *** analysis based on Apoe^(KO)Asf1a^(ECKO) mice in the atherosclerosis model confirmed the involvement of H3K18la in atherosclerosis and found that endotheliumspecific ASF1A deficiency inhibited EndMT and alleviated atherosclerosis *** of glycolysis by pharmacologic inhibition and advanced PROTAC attenuated H3K18la,SNAI1 transcription,and EndMT-induced *** study illustrates precise crosstalk between metabolism and epigenetics via H3K18la by the P300/ASF1A molecular complex during EndMT-induced atherogenesis,which provides emerging therapies for atherosclerosis.

关键词： Histone lactylation Atherosclerosis Endothelial-tomesenchymal transition ASF1A SNAI1 Endothelial dysfunction Lactate Epigenetic

Histamine H1 Receptor in Basal Forebrain Cholinergic Circuit:A Novel Target for the Negative Symptoms of Schizophrenia?

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Neuroscience Bulletin 2022年第5期38卷 558-560页

作者： Shuangshuang Wu Chenshu Gao Feng Han Heming Cheng key laboratory of Neuropharmacology and Translational medicine of Zhejiang Province School of Pharmaceutical SciencesZhejiang Chinese Medical UniversityHangzhou 310053China key laboratory of cardiovascular and cerebrovascular medicine School of PharmacyNanjing Medical UniversityNanjing 211166China

Schizophrenia is a common and severe mental disorder with a lifetime prevalence of~1%[1]Apart from the typical positive symptoms,such as hallucinations and delusions,which mainly make patients seek medication,60%-70%of patients are tortured by negative symptoms(*** and alogia)and cognitive deficits that impose a long-term burden on patients[2].

关键词： Schizophrenia patients medication

Epigenetic regulation of the inflammatory response in stroke

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Neural Regeneration Research 2025年第11期20卷 3045-3062页

作者： Jingyi Liang Fei Yang Zixiao Li Qian Li School of Basic Medical Sciences Capital Medical UniversityBeijingChina Department of Neurobiology School of Basic Medical SciencesCapital Medical UniversityBeijingChina laboratory for Clinical medicine Beijing Key Laboratory of Neural Regeneration and RepairCapital Medical UniversityBeijingChina Department of Neurology Beijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical Research Center for Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina National Center for Healthcare Quality Management in Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Chinese Institute for Brain Research BeijingChina Research Unit of Artificial Intelligence in cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina Beijing Engineering Research Center of Digital Healthcare for Neurological Diseases BeijingChina Department of Biochemistry and Molecular Biology School of Basic Medical SciencesCapital Medical UniversityBeijingChina Beijing key laboratory of Cancer Invasion and Metastasis Research Capital Medical UniversityBeijingChina

Stroke is classified as ischemic or hemorrhagic,and there are few effective treatments for either *** mechanisms play a critical role in secondary brain injury following a stroke,which manifests as cytokine release,blood–brain barrier disruption,neuronal cell death,and ultimately behavioral *** the inflammatory response has been shown to mitigate this cascade of events in experimental stroke ***,in clinical trials of anti-inflammatory agents,longterm immunosuppression has not demonstrated significant clinical benefits for *** may be attributable to the dichotomous roles of inflammation in both tissue injury and repair,as well as the complex pathophysiologic inflammatory processes in *** acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic *** agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of ***,epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke *** this review,we summarize current findings on the epigenetic regulation of the inflammatory response in stroke,focusing on key signaling pathways including nuclear factor-kappa B,Janus kinase/signal transducer and activator of transcription,and mitogen-activated protein kinase as well as inflammasome *** also discuss promising molecular targets for stroke *** evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke,leading to improved post-stroke outcomes.

关键词： DNA methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding RNA RNA methylation subarachnoid hemorrhage treatment

What is the new target inhibiting the progression of Alzheimer's disease?

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Neural Regeneration Research 2013年第21期8卷 1938-1947页

作者： Lin Zhang Jing Yang Yunpeng Cao Department of Neurology First Affiliated Hospital of China Medical University Provincial key laboratory of cardiovascular and cerebrovascular Drug Basic Research Liaoning Medical University

To stop the progression of Alzheimer＇s disease in the early stage, it is necessary to identify new therapeutic targets. We examined striatal-enriched phosphatase 61 expression in the brain tissues of 12-month-old APPswe/PSEN1dE9 transgenic mice. Immunohistochemistry showed that striatal-enriched phosphatase 61 protein expression was significantly increased but phosphorylated N-methyl-D-aspartate receptor 2B levels were significantly decreased in the cortex and hippocampus of APPswe/PSEN1dE9 transgenic mice. Western blotting of a cell model of Alzheimer＇s disease consisting of amyloid-beta peptide （1-42）-treated C57BL/6 mouse cortical neurons in vitro showed that valeric acid （AP5）, an N-methyl-D-aspartate receptor antagonist, significantly inhibited amyloidbeta 1-42-induced increased activity of striatal-enriched phosphatase 61. In addition, the phosphorylation of N-methyl-D-aspartate receptor 2B at Tyr1472 was impaired in amyloid-beta 1-42-treated cortical neurons, but knockdown of striatal-enriched phosphatase 61 enhanced the phosphorylation of N-methyl-D-aspartate receptor 2B. Collectively, these findings indicate that striatal-enriched phosphatase 61 can disturb N-methyl-D-aspartate receptor transport and inhibit the progression of learning and study disturbances induced by Alzheimer＇s disease. Thus, striatal-enriched phosphatase 61 may represent a new target for inhibiting the progression of Alzheimer＇s disease.

关键词： neural regeneration brain injury neurodegeneration Alzheimer’s disease striatal-enriched phosphatase 61 amyloid-beta peptide N-methyl-D-aspartate receptor GluN2B RNA interference immunohistochemistry western blot neuroregeneration