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| 1 | Reprogrammed mouse astrocytes retain a“memory”of tissue origin and possess more tendencies for neuronal differentiation than reprogrammed mouse embryonic fibroblasts显示文摘Direct reprogramming of a variety of somatic cells with the transcription factors Oct4(also called Pou5f1),Sox2 with either Klf4 and Myc or Lin28 and Nanog generates the induced pluripotent stem cells(iPSCs)with marker similarity to embryonic stem cells.However,the difference between iPSCs derived from different origins is unclear.In this study,we hypothesized that reprogrammed cells retain a“memory”of their origins and possess additional potential of related tissue differentiation.We reprogrammed primary mouse astrocytes via ectopic retroviral expression of OCT3/4,Sox2,Klf4 and Myc and found the iPSCs from mouse astrocytes expressed stem cell markers and formed teratomas in SCID mice containing derivatives of all three germ layers similar to mouse embryonic stem cells besides semblable morphologies.To test our hypothesis,we compared embryonic bodies(EBs)formation and neuronal differentiation between iPSCs from mouse embryonic fibroblasts(MEFsiPSCs)and iPSCs from mouse astrocytes(mAsiPSCs).We found that mAsiPSCs grew slower and possessed more potential for neuronal differentiation compared to MEFsiPSCs.Our results suggest that mAsiPSCs retain a“memory”of the central nervous system,which confers additional potential upon neuronal differentiation. | Changhai Tian Yongxiang Wang Lijun Sun Kangmu Ma Jialin C.Zheng | 2011 | Protein & Cell2011，2，2： | 6 |
| 2 | Proteolytic processing of SDF-1α by matrix metalloproteinase-2 impairs CXCR4 signaling and reduces neural progenitor cell migration显示文摘Neural stem cells and neural progenitor cells(NPCs)exist throughout life and are mobilized to replace neurons,astrocytes and oligodendrocytes after injury.Str-omal cell-derived factor 1(SDF-1,now named CXCL12)and its receptor CXCR4,an α-chemokine receptor,are critical for NPC migration into damaged areas of the brain.Our previous studies demonstrated that immune activated and/or HIV-1-infected human monocyte-derived-macrophages(MDMs)induced a substantial increase of SDF-1 production by human astrocytes.However,matrix metalloproteinase(MMP)-2,a protein up-regulated in HIV-1-infected macrophages,is able to cleave four amino acids from the N-terminus of SDF-1,resulting in a truncated SDF-1(5-67).In this study,we investigate the diverse signaling and function induced by SDF-1α and SDF-1(5-67)in human cortical NPCs.SDF-1(5-67)was generated by incubating human recombinant SDF-1α with MMP-2 followed by protein determination via mass spectrometry,Western blotting and ELISA.SDF-1α induced time-dependent phosphorylation of extracellular signal-regulated kinases(ERK)1/2,Akt-1,and diminished cyclic adenosine monophosphate(cAMP).In contrast,SDF-1(5-67)failed to induce these signaling.SDF-1α activation of CXCR4 induced migration of NPCs,an effect that is dependent on ERK1/2 and Akt-1 pathways;whereas SDF-1(5-67)failed to induce NPC migration.This observation provides evidence that MMP-2 may affect NPC migration through post-translational processing of SDF-1α. | Hui Peng Yumei Wu Zhiyuan Duan Pawel Ciborowski Jialin C.Zheng | 2012 | Protein & Cell2012，3，11： | 3 |
| 3 | The Herpes Simplex Virus Type 1 Infected Cell Protein 22显示文摘As one of the immediate-early(IE)proteins of herpes simplex virus type 1(HSV-1),ICP22 is a multifunctional viral regulator that localizes in the nucleus of infected cells.It is required in experimental animal systems and some nonhuman cell lines,but not in Vero or HEp-2 cells.ICP22 is extensively phosphorylated by viral and cellular kinases and nucleotidylylated by casein kinase Ⅱ.It has been shown to be required for efficient expression of early(E)genes and a subset of late(L)genes.ICP22,in conjunction with the UL13 kinase,mediates the phosphorylation of RNA polymerase Ⅱ.Both ICP22 and UL13 are required for the activation of cdc2,the degradation of cyclins A and B and the acquisition of a new cdc2 partner,the UL42 DNA polymerase processivity factor.The cdc2-UL42 complex mediates postranscriptional modification of topoisomerase Ⅱα in an ICP22-dependent manner to promote L gene expression.In addition,ICP22 interacts with cdk9 in a Us3 kinase dependent fashion to phosphorylate RNA polymerase Ⅱ. | Alan C.ZHENG | 2010 | Virologica Sinica2010，25，1： | 2 |
| 4 | Direct conversion of mouse astrocytes into neural progenitor cells and specific lineages of neurons显示文摘Background:Cell replacement therapy has been envisioned as a promising treatment for neurodegenerative diseases.Due to the ethical concerns of ESCs-derived neural progenitor cells(NPCs)and tumorigenic potential of iPSCs,reprogramming of somatic cells directly into multipotent NPCs has emerged as a preferred approach for cell transplantation.Methods:Mouse astrocytes were reprogrammed into NPCs by the overexpression of transcription factors(TFs)Foxg1,Sox2,and Brn2.The generation of subtypes of neurons was directed by the force expression of cell-type specific TFs Lhx8 or Foxa2/Lmx1a.Results:Astrocyte-derived induced NPCs(AiNPCs)share high similarities,including the expression of NPC-specific genes,DNA methylation patterns,the ability to proliferate and differentiate,with the wild type NPCs.The AiNPCs are committed to the forebrain identity and predominantly differentiated into glutamatergic and GABAergic neuronal subtypes.Interestingly,additional overexpression of TFs Lhx8 and Foxa2/Lmx1a in AiNPCs promoted cholinergic and dopaminergic neuronal differentiation,respectively.Conclusions:Our studies suggest that astrocytes can be converted into AiNPCs and lineage-committed AiNPCs can acquire differentiation potential of other lineages through forced expression of specific TFs.Understanding the impact of the TF sets on the reprogramming and differentiation into specific lineages of neurons will provide valuable strategies for astrocyte-based cell therapy in neurodegenerative diseases. | Kangmu Ma Xiaobei Deng Xiaohuan Xia Zhaohuan Fan Xinrui Qi Yongxiang Wang Yuju Li Yizhao Ma Qiang Chen Hui Peng Jianqing Ding Chunhong Li Yunlong Huang Changhai Tian Jialin C.Zheng | 2018 | Translational Neurodegeneration2018，7，1： | 2 |
| 5 | Exergy cost analysis of a coal fired power plant based on structural theory of thermoeconomics显示文摘 | Zhang C Y.Wang C.Zheng X.Lou | | 0，，07： | 1 |
| 6 | Hydrogen permeation behavior and corrosion monitoring of steel in cyclic wet–dry atmospheric environment显示文摘 | C.Zheng Y.Huang C.Huo Q.Yu | 2007 | Materials and Corrosion2007，，9： | 1 |
| 7 | Kinetic energy harvesting using piezoelectric and electromagnetic technologies显示文摘 | A.Khaligh P.Zeng C.Zheng | | 0，，： | 1 |
| 8 | Extracellular vesicles,from the pathogenesis to the therapy of neurodegenerative diseases显示文摘Extracellular vesicles(EVs)are small bilipid layer-enclosed vesicles that can be secreted by all tested types of brain cells.Being a key intercellular communicator,EVs have emerged as a key contributor to the pathogenesis of various neurodegenerative diseases(NDs)including Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis,and Huntington’s disease through delivery of bioactive cargos within the central nervous system(CNS).Importantly,CNS cell-derived EVs can be purified via immunoprecipitation,and EV cargos with altered levels have been identified as potential biomarkers for the diagnosis and prognosis of NDs.Given the essential impact of EVs on the pathogenesis of NDs,pathological EVs have been considered as therapeutic targets and EVs with therapeutic effects have been utilized as potential therapeutic agents or drug delivery platforms for the treatment of NDs.In this review,we focus on recent research progress on the pathological roles of EVs released from CNS cells in the pathogenesis of NDs,summarize findings that identify CNS-derived EV cargos as potential biomarkers to diagnose NDs,and comprehensively discuss promising potential of EVs as therapeutic targets,agents,and drug delivery systems in treating NDs,together with current concerns and challenges for basic research and clinical applications of EVs regarding NDs. | Xiaohuan Xia Yi Wang Jialin C.Zheng | 2022 | Translational Neurodegeneration2022，11，1： | 1 |
| 9 | Thermoeconomic operation optimization of a coalfired powerplant显示文摘 | Xiong J H.Zhao C.Zhang C.Zheng P.B.Luh | | 0，，01： | 1 |
| 10 | 查看详情显示文摘 | Z.Guo C.Zheng B.Shi | | 0，，03： | 1 |
| 11 | Thermoeconomic diagnosis of a coal fired power plant显示文摘 | Zhang C S.Chen C.Zheng X.Lou | | 0，，02： | 1 |
| 12 | Emerging roles of extracellular vesicles in mediating RNA virus infection显示文摘The sudden outbreak of COVID-19 has once again shrouded people in the enormous threat of RNA virus.Extracellular vesicles(EVs),eukaryotic cells-derived small bi-layer vesicles mainly consisting of exosomes and microvesicles,share many properties with RNA viruses including structure,size,generation,and uptake.Emerging evidence has implicated the involvement of EVs in the pathogenesis of infectious diseases induced by RNA viruses.EVs can transfer viral receptors(e.g.,ACE 2 and CD9)to recipient cells to facilitate viral infection,directiy transport infectious viral particles to adjacent cells for virus spreading,and mask viruses with a host structure to escape immune surveillance.Here,w e examine the current status of EVs to summarize their roles in mediating RNA virus infection,together with a comprehensive discussion of the underlying mechanisms. | Xiaohuan Xia Yi Wang Jialin C.Zheng | 2021 | Fundamental Research2021，1，2： | 0 |
| 13 | Mechanical properties of 65Mn chiral structure with three ligaments显示文摘Chiral honeycomb structures have been developed in recent years, showing excellent mechanical properties, including in-plane deformation and out-of-plane bearing and vibration isolation. In this study, the 65Mn chiral structure with three ligaments was modeled and analyzed using the finite element (FE) method. The effects of the dimensionless ligament length and dimensionless ligament thickness on the in-plane equivalent elastic modulus, equivalent Poisson's ratio, and out-of-plane shear modulus were studied. The numerical results indicate that increase of the dimensionless ligament length leads to decrease of the equivalent elastic modulus and increase of the equivalePoisson's ratio, whereas the out-of-plane equivalent shear modulus decreases. The results also indicate that increase of the dimensionless ligament thickness leads to in crease of the equivalent elastic modulus, whereas the equivalent Poisson's ratio remains nearly unchanged and the out-of-plane equivalent shear modulus shows a linear in crease. The numerical results are verified by comparis on with published experime ntal data. These results will provide a reference for the application of chiral structures with three ligaments in the aerospace field. | X.W.Su D.M.Zhu C.Zheng M.M.Tomovic | 2019 | Acta Mechanica Sinica2019，35，1： | 0 |
| 14 | Microglial glutaminase 1 mediates chronic restraint stress-induced depression-like behaviors and synaptic damages显示文摘Dear Editor,Major depressive disorder(MDD)is one of the most common psychiatric illnesses that significantly increase the risk of suicide.1 Stress-triggered dysfunctions of microglia have been identified as a commonly occurred pathological feature of MDD.1–3 Microglial dysfunction contributes to the pathogenesis of MDD via immunoresponses/neuroinflammation-mediated neural damage and pathological synapse loss-mediated neural circuit disruption.1 Although the involvement of microglia in MDD has been widely investigated,the molecular mechanisms underlying microglial dysfunction remain largely unknown.Recently,we identified glutaminase 1(Gls1)as one key protein that participates in microglial dysfunction.4–6 Gls1 catalyzes the hydrolysis of glutamine to produce glutamate in the brain.4 Besides its well-known role in excitatory neurotoxicity,we found Gls1 up-regulation in microglia in animal models of Alzheimer’s disease and ischemic stroke.4,7 Gls1 activates microglia to overproduce cytokines and release inflammatory extracellular vesicles,therefore leading to neuroinflammation in animal models of Alzheimer’s disease and ischemic stroke.4–6 More importantly,Gls1 has been found to be up-regulated in the brains of MDD patients,and microglial Gls1 deficiency mitigated LPS-induced depression-like behaviors.8 However,LPS exposure is not an appropriate model to mimic MDD phenotypes,leaving the involvement of Gls1 in MDD an undetermined question. | Huili Chen Shengyang Fu Xiangyu Li Meng Shi Jiazhen Qian Shu Zhao Ping Yuan Lu Ding Xiaohuan Xia Jialin C.Zheng | 2024 | Signal Transduction and Targeted Therapy2024，9，1： | 0 |
| 15 | Translational Neurodegeneration in the era of fast growing international brain research显示文摘Another year has flown by and we have entered 2022.The challenges in 2021 have continued to occur as we unceasingly fight against the pandemic.2021 will be remembered for the world’s perseverance and dedication to overcome extremely adverse circumstances.At the beginning of 2022,we are celebrating the 10th birthday of our journal,Translational Neurodegeneration(TN).Inaugurated in 2011 under the editorship and leader-ship of Dr.Shengdi Chen,our mission is to promote and foster rapid conversion of basic science research to clinical applications by offering a high-visibility forum for groundbreaking translational research in neurodegenera-tive diseases and to ultimately benefit not only patients but also societies. | Jialin C.Zheng Shengdi Chen | 2022 | Translational Neurodegeneration2022，11，1： | 0 |
| 16 | Neural stem cell-derived extracellular vesicles mitigate Alzheimer’s disease-like phenotypes in a preclinical mouse model显示文摘Dear Editor,Alzheimer’s disease(AD)is the most common neurodegenerative disorder and the No.1 cause of dementia in elderly with no effective treatments.1 The application of stem cell-derived extracellular vesicles(EVs)has emerged as a promising therapeutic strategy for AD.2 EVs are small bilipid layer-enclosed vesicles that display blood-brain barrier(BBB)penetrating ability and similar potency to their parental cells. | Ge Gao Congcong Li Yizhao Ma Zhanping Liang Yun Li Xiangyu Li Shengyang Fu Yi Wang Xiaohuan Xia Jialin C.Zheng | 2023 | Signal Transduction and Targeted Therapy2023，8，7： | 0 |
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