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Chinese Journal of Natural Medicines 2023年第3期21卷 172-184页

作者： LI Qiang GUO Lei WANG Jian TAO Shengjun JIN Peisheng Department of Plastic Surgery the Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221000China

Mesenchymal stem cell(MSC)-derived exosomes(Exos)were reported to a prospective candidate in accelerating diabetic wound healing due to their pro-angiogenic effect.MSCs pretreated with chemistry or biology factors were reported to advance the biological activities of MSC-derived exosomes.Hence,this study was designed to explore whether exosomes derived from human umbilical cord MSCs(hucMSCs)preconditioned with Nocardia rubra cell wall skeleton(Nr-CWS)exhibited superior proangiogenic effect on diabetic wound repair and its underlying molecular mechanisms.The results showed that Nr-CWS-Exos facilitated the proliferation,migration and tube formation of endothelial cells in vitro.In vivo,Nr-CWS-Exos exerted great effect on advancing wound healing by facilitating the angiogenesis of wound tissues compared with Exos.Furthermore,the expression of circIARS1 increased after HUVECs were treated with Nr-CWS-Exos.CircIARS1 promoted the pro-angiogenic effects of Nr-CWS-Exos on endothelial cells via the miR-4782-5p/VEGFA axis.Taken together,those data reveal that exosomes derived from Nr-CWS-pretreated MSCs might serve as an underlying strategy for diabetic wound treatment through advancing the biological function of endothelial cells via the circIARS1/miR-4782-5p/VEGFA axis.

关键词： Exosomes Nocardia rubra cell wall skeleton(Nr-CWS) circIARS1 Angiogenesis Mesenchymal stromal cells

Blunt dopamine transmission due to decreased GDNF in the PFC evokes cognitive impairment in Parkinson’s disease

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Neural Regeneration Research 2023年第5期18卷 1107-1117页

作者： Chuan-Xi Tang Jing Chen Kai-Quan Shao Ye-Hao Liu Xiao-Yu Zhou Cheng-Cheng Ma Meng-Ting Liu Ming-Yu Shi Piniel Alphayo Kambey Wei Wang Abiola Abdulrahman Ayanlaja Yi-Fang Liu Wei Xu Gang Chen Jiao Wu Xue Li Dian-Shuai Gao Department of Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Experinental Teaching Center of Morphology Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Affiliated Suqian Hospital of Xuzhou Medical UniversitySuqianJiangsu ProvinceChina Department of Rehabilitation Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Medicine Jiangnan UniversityWuxiJiangsu ProvinceChina Department of Nursing Care the Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Studies have found that the absence of glial cell line-derived neurotrophic factor may be the primary risk factor for Parkinson’s disease. However, there have not been any studies conducted on the potential relationship between glial cell line-derived neurotrophic factor and cognitive performance in Parkinson’s disease. We first performed a retrospective case-control study at The Affiliated Hospital of Xuzhou Medical University between September 2018 and January 2020 and found that a decreased serum level of glial cell line-derived neurotrophic factor was a risk factor for cognitive disorders in patients with Parkinson’s disease. We then established a mouse model of Parkinson’s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and analyzed the potential relationships among glial cell line-derived neurotrophic factor in the prefrontal cortex, dopamine transmission, and cognitive function. Our results showed that decreased glial cell line-derived neurotrophic factor in the prefrontal cortex weakened dopamine release and transmission by upregulating the presynaptic membrane expression of the dopamine transporter, which led to the loss and primitivization of dendritic spines of pyramidal neurons and cognitive impairment. In addition, magnetic resonance imaging data showed that the long-term lack of glial cell line-derived neurotrophic factor reduced the connectivity between the prefrontal cortex and other brain regions, and exogenous glial cell line-derived neurotrophic factor significantly improved this connectivity. These findings suggested that decreased glial cell line-derived neurotrophic factor in the prefrontal cortex leads to neuroplastic degeneration at the level of synaptic connections and circuits, which results in cognitive impairment in patients with Parkinson’s disease.

关键词： cognitive impairment degree centrality dendritic spine dopamine transmission dopamine transporter glial cell line-derived neurotrophic factor Parkinson’s disease prefrontal cortex synaptic plasticity

Long noncoding RNA Pvt1 promotes the proliferation and migration of Schwann cells by sponging microRNA-214 and targeting c-Jun following peripheral nerve injury

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Neural Regeneration Research 2023年第5期18卷 1147-1153页

作者： Bin Pan Di Guo Li Jing Ke Li Xin Li Gen Li Xiao Gao Zhi-Wen Li Wei Zhao Hu Feng Meng-Han Cao Department of Orthopedics The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Orthopedics The Second Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Imaging Xuzhou Central HospitalXuzhouJiangsu ProvinceChina College of Extended Education Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Orthopedics Kuitun HospitalYili Kazak Autonomous PrefectureXinjiang Uygur Autonomous RegionChina Center of Clinical Oncology The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Research has shown that long-chain noncoding RNAs(lncRNAs) are involved in the regulation of a variety of biological processes, including peripheral nerve regeneration, in part by acting as competing endogenous RNAs. c-Jun plays a key role in the repair of peripheral nerve injury. However, the precise underlying mechanism of c-Jun remains unclear. In this study, we performed microarray and bioinformatics analysis of mouse crush-injured sciatic nerves and found that the lncRNA Pvt1 was overexpressed in Schwann cells after peripheral nerve injury. Mechanistic studies revealed that Pvt1 increased c-Jun expression through sponging miRNA-214. We overexpressed Pvt1 in Schwann cells cultured in vitro and found that the proliferation and migration of Schwann cells were enhanced, and overexpression of miRNA-214 counteracted the effects of Pvt1 overexpression on Schwann cell proliferation and migration. We conducted in vivo analyses and injected Schwann cells overexpressing Pvt1 into injured sciatic nerves of mice. Schwann cells overexpressing Pvt1 enhanced the regeneration of injured sciatic nerves following peripheral nerve injury and the locomotor function of mice was improved. Our findings reveal the role of lncRNAs in the repair of peripheral nerve injury and highlight lncRNA Pvt1 as a novel potential treatment target for peripheral nerve injury.

关键词： cell migration ceRNA c-Jun lncRNA microarray miR-214 nerve regeneration peripheral nerve injury Pvt1 Schwann cells

Targeting the COP9 signalosome for cancer therapy

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Cancer Biology & Medicine 2022年第5期19卷 573-590页

作者： Wenqi Du Ruicheng Zhang Bilal Muhammad Dongsheng Pei Department of Pathology Xuzhou Medical UniversityXuzhou 221004China Department of Human Anatomy Xuzhou Medical UniversityXuzhou 221004China Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221006China

The COP9 signalosome(CSN)is a highly conserved protein complex composed of 8 subunits(CSN1 to CSN8).The individual subunits of the CSN play essential roles in cell proliferation,tumorigenesis,cell cycle regulation,DNA damage repair,angiogenesis,and microenvironmental homeostasis.The CSN complex has an intrinsic metalloprotease that removes the ubiquitin-like activator NEDD8 from cullin-RING ligases(CRLs).Binding of neddylated CRLs to CSN is sensed by CSN4 and communicated to CSN5 with the assistance of CSN6,thus leading to the activation of deneddylase.Therefore,CSN is a crucial regulator at the intersection between neddylation and ubiquitination in cancer progression.Here,we summarize current understanding of the roles of individual CSN subunits in cancer progression.Furthermore,we explain how the CSN affects tumorigenesis through regulating transcription factors and the cell cycle.Finally,we discuss individual CSN subunits as potential therapeutic targets to provide new directions and strategies for cancer therapy.

关键词： COP9 signalosome ubiquitin cullin-RING ligases cell proliferation tumorigenesis

SENP2-mediated SERCA2a deSUMOylation increases calcium overload in cardiomyocytes to aggravate myocardial ischemia/reperfusion injury

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Chinese medical Journal 2023年第20期136卷 2496-2507页

作者： Yuanyuan Luo Shuaishuai Zhou Tao Xu Wanling Wu Pingping Shang Shuai Wang Defeng Pan Dongye Li Department of Cardiology The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu 221006China Institute of Cardiovascular Disease Research Xuzhou Medical UniversityXuzhouJiangsu 221002China

Background:Sarcoplasmic reticulum calcium ATPase 2a(SERCA2a)is a key protein that maintains myocardial Ca2+homeostasis.The present study aimed to investigate the mechanism underlying the SERCA2a-SUMOylation(small ubiquitinlike modifier)process after ischemia/reperfusion injury(I/RI)in vitro and in vivo.Methods:Calcium transient and systolic/diastolic function of cardiomyocytes isolated from Serca2a knockout(KO)and wildtype mice with I/RI were compared.SUMO-relevant protein expression and localization were detected by quantitative real-time PCR(RT-qPCR),Western blotting,and immunofluorescence in vitro and in vivo.Serca2a-SUMOylation,infarct size,and cardiac function of Senp1 or Senp2 overexpressed/suppressed adenovirus infected cardiomyocytes,were detected by immunoprecipitation,triphenyltetrazolium chloride(TTC)-Evans blue staining,and echocardiography respectively.Results:The results showed that the changes of Fura-2 fluorescence intensity and contraction amplitude of cardiomyocytes decreased in the I/RI groups and were further reduced in the Serca2a KO+I/RI groups.Senp1 and Senp2 messenger ribose nucleic acid(mRNA)and protein expression levels in vivo and in cardiomyocytes were highest at 6 h and declined at 12 h after I/RI.However,the highest levels in HL-1 cells were recorded at 12 h.Senp2 expression increased in the cytoplasm,unlike that of Senp1.Inhibition of Senp2 protein reversed the I/RI-induced Serca2a-SUMOylation decline,reduced the infarction area,and improved cardiac function,while inhibition of Senp1 protein could not restore the above indicators.Conclusion:I/RI activated Senp1 and Senp2 protein expression,which promoted Serca2a-deSUMOylation,while inhibition of Senp2 expression reversed Serca2a-SUMOylation and improved cardiac function.

关键词： Myocardial ischemia Reperfusion injury Sarcoplasmic reticulum calcium-transporting ATPases Sentrin/SUMOspecific protease Calcium overload

Overexpression of vascular endothelial growth factor enhances the neuroprotective effects of bone marrow mesenchymal stem cell transplantation in ischemic stroke

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Neural Regeneration Research 2023年第6期18卷 1286-1292页

作者： Cui Liu Zhi-Xiang Yang Si-Qi Zhou Ding Ding Yu-Ting Hu Hong-Ning Yang Dong Han Shu-Qun Hu Xue-Mei Zong Institute of Emergency Rescue Medicine Emergency Centerthe Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Emergency Department of affiliated Lianyungang hospital of xuzhou medical university/The First People’s hospital of Lianyungang LianyungangLianyungangJiangsu ProvinceChina Laboratory of Emergency Medicine Second Clinical Medical College of Xuzhou Medical UniversityXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Key Laboratory of Brain Diseases Bioinformation Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Although bone marrow mesenchymal stem cells(BMSCs)might have therapeutic potency in ischemic stroke,the benefits are limited.The current study investigated the effects of BMSCs engineered to overexpress vascular endothelial growth factor(VEGF)on behavioral defects in a rat model of transient cerebral ischemia,which was induced by middle cerebral artery occlusion.VEGF-BMSCs or control grafts were injected into the left striatum of the infarcted hemisphere 24 hours after stroke.We found that compared with the stroke-only group and the vehicle-and BMSCs-control groups,the VEGF-BMSCs treated animals displayed the largest benefits,as evidenced by attenuated behavioral defects and smaller infarct volume 7 days after stroke.Additionally,VEGF-BMSCs greatly inhibited destruction of the blood-brain barrier,increased the regeneration of blood vessels in the region of ischemic penumbra,and reducedneuronal degeneration surrounding the infarct core.Further mechanistic studies showed that among all transplant groups,VEGF-BMSCs transplantation induced the highest level of brain-derived neurotrophic factor.These results suggest that BMSCs transplantation with vascular endothelial growth factor has the potential to treat ischemic stroke with better results than are currently available.

关键词： bone marrow mesenchymal stem cell brain-derived neurotrophic factor CD31 microtubule associated protein 2 middle cerebral artery occlusion stroke transplantation vascular endothelial growth factor

β2-Microglobulin exacerbates neuroinflammation,brain damage,and cognitive impairment after stroke in rats

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Neural Regeneration Research 2023年第3期18卷 603-608页

作者： Feng Chen Jing Liu Fa-Qiang Li Shuai-Shuai Wang Yan-Yan Zhang Yun-Yun Lu Fang-Fang Hu Rui-Qin Yao Department of Neurology Xuzhou Cancer HospitalXuzhouJiangsu ProvinceChina Department of Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Xuzhou No.1 People’s Hospitalthe Affiliated Xuzhou Municipal Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

β2-Microglobulin(β2M),a component of the major histocompatibility complex class I molecule,is associated with aging-related cognitive impairment and Alzheimer’s disease.Although upregulation ofβ2M is considered to be highly related to ischemic stroke,the specific role and underlying mechanistic action ofβ2M are poorly understood.In this study,we established a rat model of focal cerebral ischemia by occlusion of the middle cerebral artery.We found thatβ2M levels in the cerebral spinal fluid,serum,and brain tissue were significantly increased in the acute period but gradually decreased during the recovery period.RNA interference was used to inhibitβ2M expression in the acute period of cerebral stroke.Tissue staining with 2,3,5-triphenyltetrazolium chloride and evaluation of cognitive function using the Morris water maze test demonstrated that decreasedβ2M expression in the ischemic penumbra reduced infarct volume and alleviated cognitive deficits,respectively.Notably,glial cell,caspase-1(p20),and Nod-like receptor pyrin domain containing 3(NLRP3)inflammasome activation as well as production of the inflammatory cytokines interleukin-1β,interleukin-6,and tumor necrosis factor-αwere also effectively inhibited byβ2M silencing.These findings suggest thatβ2M participates in brain injury and cognitive impairment in a rat model of ischemic stroke through activation of neuroinflammation associated with the NLRP3 inflammasome.

关键词： cognitive impairment cognitive improvement glial activation infarct volume ischemia middle cerebral artery occlusion neuroinflammation NLRP3 inflammasome stroke β2 microglobulin

Protective mechanism of quercetin in alleviating sepsis-related acute respiratory distress syndrome based on network pharmacology and in vitro experiments

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World Journal of Emergency Medicine 2024年第2期15卷 111-120页

作者： Weichao Ding Wei Zhang Juan Chen Mengmeng Wang Yi Ren Jing Feng Xiaoqin Han Xiaohang Ji Shinan Nie Zhaorui Sun Department of Emergency Medicine Jinling HospitalAffiliated Hospital of Medical SchoolNanjing UniversityNanjing 210002China Department of Emergency Medicine Jinling Clinical Medical College of Nanjing University of Chinese MedicineNanjing 210002China Department of Emergency Medicine the Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221002China Department of Emergency Medicine Xuzhou Municipal Hospital Affiliated to Xuzhou Medical UniversityXuzhou 221000China

BACKGROUND:Sepsis-related acute respiratory distress syndrome(ARDS)has a high mortality rate,and no effective treatment is available currently.Quercetin is a natural plant product with many pharmacological activities,such as antioxidative,anti-apoptotic,and anti-inflammatory effects.This study aimed to elucidate the protective mechanism of quercetin against sepsis-related ARDS.METHODS:In this study,network pharmacology and in vitro experiments were used to investigate the underlying mechanisms of quercetin against sepsis-related ARDS.Core targets and signaling pathways of quercetin against sepsis-related ARDS were screened and were verified by in vitro experiments.RESULTS:A total of 4,230 targets of quercetin,360 disease targets of sepsis-related ARDS,and 211 intersection targets were obtained via database screening.Among the 211 intersection targets,interleukin-6(IL-6),tumor necrosis factor(TNF),albumin(ALB),AKT serine/threonine kinase 1(AKT1),and interleukin-1β(IL-1β)were identified as the core targets.A Gene Ontology(GO)enrichment analysis revealed 894 genes involved in the inflammatory response,apoptosis regulation,and response to hypoxia.Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis identified 106 pathways.After eliminating and generalizing,the hypoxia-inducible factor-1(HIF-1),TNF,nuclear factor-κB(NF-κB),and nucleotide-binding and oligomerization domain(NOD)-like receptor signaling pathways were identified.Molecular docking revealed that quercetin had good binding activity with the core targets.Moreover,quercetin blocked the HIF-1,TNF,NF-κB,and NODlike receptor signaling pathways in lipopolysaccharide(LPS)-induced murine alveolar macrophage(MH-S)cells.It also suppressed the inflammatory response,oxidative reactions,and cell apoptosis.CONCLUSION:Quercetin ameliorates sepsis-related ARDS by binding to its core targets and blocking the HIF-1,TNF,NF-κB,and NOD-like receptor signaling pathways to reduce inflammation,cell apoptosis,and oxidative stress.

关键词： Quercetin Sepsis-related acute respiratory distress syndrome Network pharmacology

The Link between Exposure to Phthalates and Type 2 Diabetes Mellitus:A Study Based on NHANES Data and Bioinformatic Analysis

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生物医学与环境科学:英文版 2023年第9期36卷 892-896页

作者： LIU Xue Kui SI Shan Wen YE Yan LI Jia Yi LYU He He MA Ya Mei ZOU Cai Yan SUN Hao Jie XUE Lei XU Wei GENG Hou Fa LIANG Jun Department of Endocrinology Xuzhou Central hospitalXuzhou 221009JiangsuChina xuzhou medical university Affiliated Xuzhou Clinical College of Xuzhou Medical UniversityXuzhou 221009JiangsuChina Graduate School of Bengbu medical College Bengbu 233000AnhuiChina Department of Emergency Xuzhou Central HospitalXuzhou 221009JiangsuChina

Insulin resistance is closely associated with metabolic disorders and the pathogenesis of type 2 diabetes mellitus(T2DM).Accumulating evidence suggests that excess fatty acids due to inappropriate lipolysis increase the risk of insulin resistance,which,in turn,stimulates hyperinsulinemia,worsens metabolism,and leads to insulin resistance due to impairedβ-cell function.

关键词： metabolism impaired function.

BYSL contributes to tumor growth by cooperating with the mTORC2 complex in gliomas

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Cancer Biology & Medicine 2021年第1期18卷 88-104页

作者： Shangfeng Gao Zhuang Sha Junbo Zhou Yihao Wu Yunnong Song Cheng Li Xuejiao Liu Tong Zhang Rutong Yu Institute of Nervous System Diseases Xuzhou Medical UniversityDepartment of NeurosurgeryThe Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221002China

Objective:BYSL,which encodes the Bystin protein in humans,is upregulated in reactive astrocytes following brain damage and/or inflammation.We aimed to determine the role and mechanism of BYSL in glioma cell growth and survival.Methods:BYSL expression in glioma tissues was measured by quantitative real-time PCR,Western blot,and immunohistochemistry.In vitro assays were performed to assess the role of BYSL in cell proliferation and apoptosis.Protein interactions and co-localization were determined by co-immunoprecipitation and double immunofluorescence.The expression and activity of the AKT/m TOR signaling molecules were determined by Western blot analysis,and the role of BYSL in glioma growth was confirmed in an orthotopic xenograft model.Results:The BYSL m RNA and protein levels were elevated in glioma tissues.Silencing BYSL inhibited glioma cell proliferation,impeded cell cycle progression,and induced apoptosis,whereas overexpressing BYSL protein led to the opposite effects.We identified a complex consisting of BYSL,RIOK2,and m TOR,and observed co-localization and positive correlations between BYSL and RIOK2 in glioma cells and tissues.Overexpressing BYSL or RIOK2 increased the expression and activity of AKT/m TOR signaling molecules,whereas downregulation of BYSL or RIOK2 decreased the activity of AKT/m TOR signaling molecules.Silencing BYSL or RIOK2 decreased the growth of the tumors and prolonged the lifespan of the animals in an orthotopic xenograft model.Conclusions:High expression of BYSL in gliomas promoted tumor cell growth and survival both in vitro and in vivo.These effects could be attributed to the association of BYSL with RIOK2 and m TOR,and the subsequent activation of AKT signaling.

关键词： Bystin glioblastoma proliferation apoptosis AKT