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Dgcr8 deletion in the primitive heart uncovered novel microRNA regulating the balance of cardiac-vascular gene program
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作者 Xi Chen Lin Wang +8 位作者 Rujin Huang Hui Qiu Peizhe Wang Daren Wu Yonglin Zhu Jia Ming Yangming Wang Jianbin Wang Jie Na 《蛋白质与细胞:英文版》 SCIE CAS CSCD 2019年第5期327-346,共20页
Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window.We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mespl cardi... Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window.We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mespl cardiovascular progenitor cells lead to the formation of extremely dilated and enlarged heart due to defective cardiomyocyte(CM)differentiation.Transcriptome analysis revealed unusual upregulation of vascular gene expression in Dgcr8 cKO hearts.Single cell RNA sequencing study further confirmed the increase of angiogenesis genes in single Dgcr8 cKO CM.We also performed global microRNA profiling of E9.5 heart for the first time,and identified that miR-541 was transiently highly expressed in E9.5 hearts.Interestingly,introducing miR-541 back into microRNA-free CMs partially rescued their defects,downregulated angiogenesis genes and significantly upregulated cardiac genes.Moreover,miR-541 can target Ctgf and inhibit endothelial function.Our results suggest that micro-RNAs are required to suppress abnormal angiogenesis gene program to maintain CM differentiation. 展开更多
关键词 MICRORNA Dgcr8 Cardiovascular PROGENITOR cells miRNA-541 Single cell RNA sequencing
Dysfunctional stem and progenitor cells impair fracture healing with age 预览
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作者 Diane R Wagner Sonali Karnik +10 位作者 Zachary J Gunderson Jeffery J Nielsen Alanna Fennimore Hunter J Promer Jonathan W Lowery M Terry Loghmani Philip S Low Todd O McKinley Melissa A Kacena Matthias Clauss Jiliang Li 《世界干细胞杂志:英文版(电子版)》 2019年第6期281-296,共16页
Successful fracture healing requires the simultaneous regeneration of both the bone and vasculature;mesenchymal stem cells (MSCs) are directed to replace the bone tissue, while endothelial progenitor cells (EPCs) form... Successful fracture healing requires the simultaneous regeneration of both the bone and vasculature;mesenchymal stem cells (MSCs) are directed to replace the bone tissue, while endothelial progenitor cells (EPCs) form the new vasculature that supplies blood to the fracture site. In the elderly, the healing process is slowed, partly due to decreased regenerative function of these stem and progenitor cells. MSCs from older individuals are impaired with regard to cell number, proliferative capacity, ability to migrate, and osteochondrogenic differentiation potential. The proliferation, migration and function of EPCs are also compromised with advanced age. Although the reasons for cellular dysfunction with age are complex and multidimensional, reduced expression of growth factors, accumulation of oxidative damage from reactive oxygen species, and altered signaling of the Sirtuin-1 pathway are contributing factors to aging at the cellular level of both MSCs and EPCs. Because of these geriatric-specific issues, effective treatment for fracture repair may require new therapeutic techniques to restore cellular function. Some suggested directions for potential treatments include cellular therapies, pharmacological agents, treatments targeting age-related molecular mechanisms, and physical therapeutics. Advanced age is the primary risk factor for a fracture, due to the low bone mass and inferior bone quality associated with aging;a better understanding of the dysfunctional behavior of the aging cell will provide a foundation for new treatments to decrease healing time and reduce the development of complications during the extended recovery from fracture healing in the elderly. 展开更多
关键词 Fracture HEALING Aging Bone Angiogenesis MESENCHYMAL STEM CELLS Endothelial PROGENITOR CELLS
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Soluble Nogo receptor 1 fusion protein protects neural progenitor cells in rats with ischemic stroke 预览
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作者 Hai-Wei He Yue-Lin Zhang +4 位作者 Bao-Qi Yu Gen Ye Wei You Kwok-fai So Xin Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1755-1764,共10页
Soluble Nogo66 receptor-Fc protein(sNgR-Fc)enhances axonal regeneration following central nervous system injury.However,the underlying mechanisms remain unclear.In this study,we investigated the effects of sNgR-Fc on ... Soluble Nogo66 receptor-Fc protein(sNgR-Fc)enhances axonal regeneration following central nervous system injury.However,the underlying mechanisms remain unclear.In this study,we investigated the effects of sNgR-Fc on the proliferation and differentiation of neural progenitor cells.The photothrombotic cortical injury model of ischemic stroke was produced in the parietal cortex of Sprague-Dawley rats.The rats with photothrombotic cortical injury were randomized to receive infusion of 400μg/kg sNgR-Fc(sNgR-Fc group)or an equal volume of phosphate-buffered saline(photothrombotic cortical injury group)into the lateral ventricle for 3 days.The effects of sNgR-Fc on the proliferation and differentiation of endogenous neural progenitor cells were examined using BrdU staining.Neurological function was evaluated with the Morris water maze test.To further examine the effects of sNgR-Fc treatment on neural progenitor cells,photothrombotic cortical injury was produced in another group of rats that received transplantation of neural progenitor cells from the hippocampus of embryonic Sprague-Dawley rats.The animals were then given an infusion of phosphate-buffered saline(neural progenitor cells group)or sNgR-Fc(sNgR-Fc+neural progenitor cells group)into the lateral ventricle for 3 days.sNgR-Fc enhanced the proliferation of cultured neural progenitor cells in vitro as well as that of endogenous neural progenitor cells in vivo,compared with phosphate-buffered saline,and it also induced the differentiation of neural progenitor cells into neurons.Compared with the photothrombotic cortical injury group,escape latency in the Morris water maze and neurological severity score were greatly reduced,and distance traveled in the target quadrant was considerably increased in the sNgR-Fc group,indicating a substantial improvement in neurological function.Furthermore,compared with phosphate-buffered saline infusion,sNgR-Fc infusion strikingly improved the survival and differentiation of grafted neural progenitor cells.Our findings show that 展开更多
关键词 NEURAL REGENERATION Nogo-66 RECEPTOR Nogo66 receptor-Fc protein NEURAL PROGENITOR cells proliferation differentiation stroke photothrombotic cortical injury transplantation NEUROLOGICAL function nerve REGENERATION
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Diffuse Intrinsic Pontine Gliomas Exhibit Cell Biological and Molecular Signatures of Fetal Hindbrain-Derived Neural Progenitor Cells
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作者 Yu Sun Cheng Xu +11 位作者 Changcun Pan Xin Chen Yibo Geng Yuliang Wu Peng Zhang Wenhao Wu Yu Wang Deling Li Zhen Wu Junting Zhang Qiaoran Xi Liwei Zhang 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第2期216-224,共9页
Diffuse intrinsic pontine glioma(DIPG) is the main cause of brain tumor-related death among children.Until now, there is still a lack of effective therapy with prolonged overall survival for this disease. A typical st... Diffuse intrinsic pontine glioma(DIPG) is the main cause of brain tumor-related death among children.Until now, there is still a lack of effective therapy with prolonged overall survival for this disease. A typical strategy for preclinical cancer research is to find out the molecular differences between tumor tissue and para-tumor normal tissue, in order to identify potential therapeutic targets. Unfortunately, it is impossible to obtain normal tissue for DIPG because of the vital functions of the pons.Here we report the human fetal hindbrain-derived neural progenitor cells(pontine progenitor cells, PPCs) as normal control cells for DIPG. The PPCs not only harbored similar cell biological and molecular signatures as DIPG glioma stem cells, but also had the potential to be immortalized by the DIPG-specific mutation H3 K27 M in vitro. These findings provide researchers with a candidate normal control and a potential medicine carrier for preclinical research on DIPG. 展开更多
关键词 Diffuse intrinsic PONTINE GLIOMA Neural PROGENITOR cells IMMORTALIZATION H3K27M SENESCENCE
Physiological and pathological effects of amyloid-β species in neural stem cell biology 预览
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作者 Adela Bernabeu-Zornoza Raquel Coronel +3 位作者 Charlotte Palmer María Monteagudo Alberto Zambrano Isabel Liste 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第12期2035-2042,共8页
Although amyloid-β peptide is considered neurotoxic, it may mediate several physiological processes during embryonic development and in the adult brain. The pathological function of amyloid-β peptide has been extens... Although amyloid-β peptide is considered neurotoxic, it may mediate several physiological processes during embryonic development and in the adult brain. The pathological function of amyloid-β peptide has been extensively studied due to its implication in Alzheimer’s disease, but its physiological function remains poorly understood. Amyloid-β peptide can be detected in non-aggregated (monomeric) and aggregated (oligomeric and fibrillary) forms. Each form has different cytotoxic and/or physiological properties, so amyloid-β peptide and its role in Alzheimer’s disease need to be studied further. Neural stem cells and neural precursor cells are good tools for the study on neurodegenerative diseases and can provide future therapeutic applications in diseases such as Alzheimer’s disease. In this review, we provide an outline of the effects of amyloid-β peptide, in monomeric and aggregated forms, on the biology of neural stem cells/neural precursor cells, and discuss the controversies. We also describe the possible molecular targets that could be implicated in these effects, especially GSK3β. A better understanding of amyloid-β peptide (both physiological and pathological), and the signaling pathways involved are essential to advance the field of Alzheimer’s disease. 展开更多
关键词 amyloid-β peptide NEURAL stem CELLS NEURAL PROGENITOR CELLS Alzheimer's disease AMYLOID precursor protein toxicity NEUROGENESIS gliogenesis GSK3β
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Single-cell analyses identify distinct and intermediate states of zebrafish pancreatic islet development
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作者 Chong-Jian Lu Xiao-Ying Fan +12 位作者 Yue-Feng Guo Zhen-Chao Cheng Ji Dong Jin-Zi Chen Lian-Yan Li Mei-Wen Wang Ze-Kai Wu Fei Wang Xiang-Jun Tong Ling-Fei Luo Fu-Chou Tang Zuo-Yan Zhu Bo Zhang 《分子细胞生物学报:英文版》 SCIE CAS CSCD 2019年第6期435-447,共13页
Pancreatic endocrine islets are vital for glucose homeostasis. However, the islet developmental trajectory and its regulatory network are not well understood. To define the features of these specification and differen... Pancreatic endocrine islets are vital for glucose homeostasis. However, the islet developmental trajectory and its regulatory network are not well understood. To define the features of these specification and differentiation processes, we isolated individual islet cells from TgBAC(neurod1:EGFP) transgenic zebrafish and analyzed islet developmental dynamics across four different embryonic stages using a single-cell RNA-seq strategy. We identified proliferative endocrine progenitors, which could be further categorized by different cell cycle phases with the G1/S subpopulation displaying a distinct differentiation potential. We identified endocrine precursors, a heterogeneous intermediate-state population consisting of lineage-primed alpha, beta and delta cells that were characterized by the expression of lineage-specific transcription factors and relatively low expression of terminally differentiation markers. The terminally differentiated alpha, beta, and delta cells displayed stage-dependent differentiation states, which were related to their functional maturation. Our data unveiled distinct states, events and molecular features during the islet developmental transition, and provided resources to comprehensively understand the lineage hierarchy of islet development at the single-cell level. 展开更多
关键词 SINGLE-CELL RNA-seq ZEBRAFISH pancreas ISLET precursor CELL PROGENITOR CELL
Decreased numbers of circulating endothelial progenitor cells are associated with hyperglycemia in patients with traumatic brain injury 预览
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作者 Hui-Jie Wei Li Liu +7 位作者 Fang-Lian Chen Dong Wang Liang Wang Zeng-Guang Wang Rong-Cai Jiang Jing-Fei Dong Jie-Li Chen Jian-Ning Zhang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第6期984-990,共7页
Hyperglycemia reduces the number of circulating endothelial progenitor cells,accelerates their senescence and impairs their function.However,the relationship between blood glucose levels and endothelial progenitor cel... Hyperglycemia reduces the number of circulating endothelial progenitor cells,accelerates their senescence and impairs their function.However,the relationship between blood glucose levels and endothelial progenitor cells in peripheral blood of patients with traumatic brain injury is unclear.In this study,101 traumatic brain injury patients admitted to the Department of Neurosurgery,Tianjin Medical University General Hospital or the Department of Neurosurgery,Tianjin Huanhu Hospital,China,were enrolled from April 2005 to March 2007.The number of circulating endothelial progenitor cells and blood glucose levels were measured at 1,4,7,14 and 21 days after traumatic brain injury by flow cytometry and automatic biochemical analysis,respectively.The number of circulating endothelial progenitor cells and blood sugar levels in 37 healthy control subjects were also examined.Compared with controls,the number of circulating endothelial progenitor cells in traumatic brain injury patients was decreased at 1 day after injury,and then increased at 4 days after injury,and reached a peak at 7 days after injury.Compared with controls,blood glucose levels in traumatic brain injury patients peaked at 1 day and then decreased until 7 days and then remained stable.At 1,4,and 7 days after injury,the number of circulating endothelial progenitor cells was negatively correlated with blood sugar levels(r=?0.147,P<0.05).Our results verify that hyperglycemia in patients with traumatic brain injury is associated with decreased numbers of circulating endothelial progenitor cells.This study was approved by the Ethical Committee of Tianjin Medical University General Hospital,China(approval No.200501)in January 2015. 展开更多
关键词 nerve REGENERATION endothelial progenitor cells VASCULAR repair VASCULAR remodeling angiogenesis NEOVASCULARIZATION blood glucose HYPERGLYCEMIA traumatic BRAIN injury MOBILIZATION suppression senescence alternative therapy BRAIN damage neural REGENERATION
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P2X7 receptor signaling during adult hippocampal neurogenesis 预览
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作者 Hannah C. Leeson Tailoi Chan-Ling +3 位作者 Michael D. Lovelace Jeremy C. Brownlie Ben J. Gu Michael W. Weible II 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1684-1694,共11页
Neurogenesis is a persistent and essential feature of the adult mammalian hippocampus.Granular neurons generated from resident pools of stem or progenitor cells provide a mechanism for the formation and consolidation ... Neurogenesis is a persistent and essential feature of the adult mammalian hippocampus.Granular neurons generated from resident pools of stem or progenitor cells provide a mechanism for the formation and consolidation of new memories.Regulation of hippocampal neurogenesis is complex and multifaceted,and numerous signaling pathways converge to modulate cell proliferation,apoptosis,and clearance of cellular debris,as well as synaptic integration of newborn immature neurons.The expression of functional P2X7 receptors in the central nervous system has attracted much interest and the regulatory role of this purinergic receptor during adult neurogenesis has only recently begun to be explored.P2X7 receptors are exceptionally versatile:in their canonical role they act as adenosine triphosphate-gated calcium channels and facilitate calcium-signaling cascades exerting control over the cell via calcium-encoded sensory proteins and transcription factor activation.P2X7 also mediates transmembrane pore formation to regulate cytokine release and facilitate extracellular communication,and when persistently stimulated by high extracellular adenosine triphosphate levels large P2X7 pores form,which induce apoptotic cell death through cytosolic ion dysregulation.Lastly,as a scavenger receptor P2X7 directly facilitates phagocytosis of the cellular debris that arises during neurogenesis,as well as during some disease states.Understanding how P2X7 receptors regulate the physiology of stem and progenitor cells in the adult hippocampus is an important step towards developing useful therapeutic models for regenerative medicine.This review considers the relevant aspects of adult hippocampal neurogenesis and explores how P2X7 receptor activity may influence the molecular physiology of the hippocampus,and neural stem and progenitor cells. 展开更多
关键词 P2X7 P2X7R adult NEUROGENESIS NEURAL stem CELLS NEURAL PROGENITOR CELLS hippocampus SGZ calcium SIGNALING PURINERGIC SIGNALING
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Sphingosine 1-phosphate induces epicardial progenitor cell differentiation into smooth muscle-like cells
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作者 Yu Li Yingrui Li +3 位作者 Xiaodong Jing Yajie Liu Bin Liu Qiang She 《生物化学与生物物理学报:英文版》 SCIE CAS CSCD 2019年第4期402-410,共9页
Epicardial progenitor cells (EpiCs) which are derived from the proepicardium have the potential to differentiate into coronary vascular smooth muscle cells during development. Whether sphingosine 1-phosphate (S1P), a ... Epicardial progenitor cells (EpiCs) which are derived from the proepicardium have the potential to differentiate into coronary vascular smooth muscle cells during development. Whether sphingosine 1-phosphate (S1P), a highly hydrophobic zwitterionic lysophospholipid in signal transduction, in duces the differe ntiati on of EpiCs is unk nown. In the present study, we dem on strated that S1P significantly induced the expression of smooth muscle cell specific markers a-smooth muscle actin and myosin heavy chain 11 in the EpiCs. And the smooth muscle cells differentiated from the EpiCs stimulated by S1P were further evaluated by gel contraction assay. To further confirm the major subtype of sphingosine 1-phosphate receptors (S1 PRs) involved in the differentiation of EpiCs, we used the agonists and antagonists of different S1PRs. The results showed that the S1 Pq/ S1P3 antagonist VPC23019 and the S1P2 antagonist JTE013 significantly attenuated EpiCs differentiation, while the S1 P-i agonist SEW2871 and antagonist W146 did not affect EpiCs differentiation. These results collectively suggested that S1P, principally through its receptor S1P3, in creases EpiCs differentiation into VSMCs and thus indicated the importance of S1P signaling in the embryonic coronary vasculature, while S1P2 plays a sec on dary role. 展开更多
关键词 EPICARDIAL PROGENITOR CELLS SPHINGOSINE 1-phosphate DIFFERENTIATION smooth muscle-like CELLS SPHINGOSINE 1-phosphate receptors
The detrimental effects of lipopolysaccharideinduced neuroinflammation on adult hippocampal neurogenesis depend on the duration of the pro-inflammatory response 预览
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作者 Martha Pérez-Domínguez Evangelina Aila-Munz +1 位作者 Eduardo Domínguez-Rivas Angélica Zepeda 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第5期817-825,共9页
Adult hippocampal neurogenesis is a finely tuned process regulated by extrinsic factors.Neuroinflammation is a hallmark of several pathological conditions underlying dysregulation of neurogenesis.In animal models,lipo... Adult hippocampal neurogenesis is a finely tuned process regulated by extrinsic factors.Neuroinflammation is a hallmark of several pathological conditions underlying dysregulation of neurogenesis.In animal models,lipopolysaccharide(LPS)-induced neuroinflammation leads to a neurogenic decrease mainly associated to the early inflammatory response.However,it is not well understood how the neuroinflammatory response progresses over time and if neurogenesis continues to be diminished during the late neuroinflammatory response.Moreover,it is unknown if repeated intermittent administration of LPS along time induces a greater reduction in neurogenesis.We administered one single intraperitoneal injection of LPS or saline or four repeated injections(one per week)of LPS or saline to young-adult mice.A cohort of new cells was labeled with three 5-bromo-2-deoxyuridine injections(one per day)4 days after the last LPS injection.We evaluated systemic and neuroinflammation-associated parameters and compared the effects of the late neuroinflammatory response on neurogenesis induced by each protocol.Our results show that 1)a single LPS injection leads to a late pro-inflammatory response characterized by microglial activation,moderate astrocytic reaction and increased interleukin-6 levels.This response correlates in time with decreased neurogenesis and 2)a repeated intermittent injection of LPS does not elicit a late pro-inflammatory response although activated microglia persists.The latter profile is not accompanied by a continued longterm hippocampal neurogenic decrease.Hereby,we provide evidence that the neuroinflammatory response is a dynamic process that progresses in a milieu-dependent manner and does not necessarily lead to a neurogenic decrease,highlighting the complex interaction between the immune system and neurogenesis. 展开更多
关键词 DENTATE GYRUS subgranular zone inflammation microglia ASTROCYTES IL-6 cytokines cell proliferation neural progenitor cells IMMATURE neurons long-term short-term adult hippocampal NEUROGENESIS
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Signal transducer and activator of transcription 3 promotes the Warburg effect possibly by inducing pyruvate kinase M2 phosphorylation in liver precancerous lesions 预览
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作者 Yang-Hui Bi Wen-Qi Han +4 位作者 Ruo-Fei Li Yun-Jiao Wang Zun-Shu Du Xue-Jiang Wang Ying Jiang 《世界胃肠病学杂志:英文版》 SCIE CAS 2019年第16期1936-1949,共14页
BACKGROUND Study shows that signal transducer and activator of transcription 3 (STAT3) can increase the Warburg effect by stimulating hexokinase 2 in breast cancer and upregulate lactate dehydrogenase A and pyruvate d... BACKGROUND Study shows that signal transducer and activator of transcription 3 (STAT3) can increase the Warburg effect by stimulating hexokinase 2 in breast cancer and upregulate lactate dehydrogenase A and pyruvate dehydrogenase kinase 1 in myeloma. STAT3 and pyruvate kinase M2 (PKM2) can also be activated and enhance the Warburg effect in hepatocellular carcinoma. Precancerous lesions are critical to human and rodent hepatocarcinogenesis. However, the underlying molecular mechanism for the development of liver precancerous lesions remains unknown. We hypothesized that STAT3 promotes the Warburg effect possibly by upregulating p-PKM2 in liver precancerous lesions in rats.AIM To investigate the mechanism of the Warburg effect in liver precancerous lesions in rats.METHODS A model of liver precancerous lesions was established by a modified Solt-Farber method. The liver pathological changes were observed by HE staining and immunohistochemistry. The transformation of WB-F344 cells induced with Nmethyl- N’-nitro-N-nitrosoguanidine and hydrogen peroxide was evaluated by the soft agar assay and aneuploidy. The levels of glucose and lactate in the tissue and culture medium were detected with a spectrophotometer. The protein levels of glutathione S-transferase-π, proliferating cell nuclear antigen (PCNA), STAT3, and PKM2 were examined by Western blot and immunofluorescence.RESULTS We found that the Warburg effect was increased in liver precancerous lesions in rats. PKM2 and p-STAT3 were upregulated in activated oval cells in liver precancerous lesions in rats. The Warburg effect, p-PKM2, and p-STAT3 expression were also increased in transformed WB-F344 cells. STAT3 activation promoted the clonal formation rate, aneuploidy, alpha-fetoprotein expression, PCNA expression, G1/S phase transition, the Warburg effect, PKM2 phosphorylation, and nuclear translocation in transformed WB-F344 cells. Moreover, the Warburg effect was inhibited by stattic, a specific inhibitor of STAT3, and further reduced in transformed WB-F344 cell 展开更多
关键词 WARBURG effect Hepatic PROGENITOR cell Signal transducer and activator of transcription 3 PYRUVATE kinase M2 LIVER PRECANCEROUS lesion
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Physiological effects of amyloid precursor protein and its derivatives on neural stem cell biology and signaling pathways involved 预览
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作者 Raquel Coronel Charlotte Palmer +4 位作者 Adela Bernabeu-Zornoza María Monteagudo Andreea Rosca Alberto Zambrano Isabel Liste 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1661-1671,共11页
The pathological implication of amyloid precursor protein(APP)in Alzheimer’s disease has been widely documented due to its involvement in the generation of amyloid-β peptide.However,the physiological functions of AP... The pathological implication of amyloid precursor protein(APP)in Alzheimer’s disease has been widely documented due to its involvement in the generation of amyloid-β peptide.However,the physiological functions of APP are still poorly understood.APP is considered a multimodal protein due to its role in a wide variety of processes,both in the embryo and in the adult brain.Specifically,APP seems to play a key role in the proliferation,differentiation and maturation of neural stem cells.In addition,APP can be processed through two canonical processing pathways,generating different functionally active fragments:soluble APP-α,soluble APP-β,amyloid-β peptide and the APP intracellular C-terminal domain.These fragments also appear to modulate various functions in neural stem cells,including the processes of proliferation,neurogenesis,gliogenesis or cell death.However,the molecular mechanisms involved in these effects are still unclear.In this review,we summarize the physiological functions of APP and its main proteolytic derivatives in neural stem cells,as well as the possible signaling pathways that could be implicated in these effects.The knowledge of these functions and signaling pathways involved in the onset or during the development of Alzheimer’s disease is essential to advance the understanding of the pathogenesis of Alzheimer’s disease,and in the search for potential therapeutic targets. 展开更多
关键词 AMYLOID precursor protein APP SOLUBLE APP alpha SOLUBLE APP BETA AMYLOID BETA peptide APP intracellular domain NEURAL stem CELLS NEURAL progenitor CELLS neurogenesis signaling pathways
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Exogenous FGF-2 improves biological activity of endothelial progenitor cells exposed to high glucose conditions
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作者 Yang Li Xue Li +4 位作者 Shilong Han Weishuai Lian Jie Cheng Xiaoyun Xie Maoquan Li 《介入医学杂志》 2018年第1期9-14,共6页
Purpose: To investigate the effects of exogenous basic fibroblast growth factor-2(FGF-2) on the biological activity of endothelial progenitor cells(EPCs) exposed to high glucose conditions. Materials and Methods: 1) B... Purpose: To investigate the effects of exogenous basic fibroblast growth factor-2(FGF-2) on the biological activity of endothelial progenitor cells(EPCs) exposed to high glucose conditions. Materials and Methods: 1) Bone marrow EPCs from C57BL/6 mice were isolated and cultured in vitro. EPC purity was identified by flow cytometry and immunofluorescence staining. 2) Apoptosis was detected by TUNEL assay. Migration and tube formation ability was detected by Transwell chamber and Matrigel assays, respectively. The expression and activation of β-catenin was detected by Western blot. 3) Doppler flowmetry was used to detect the effect of FGF2 on blood flow recovery in ischemic hind limbs of mice. Results: 1) FGF-2 treatment reversed high glucose induced growth inhibition of EPCs. FGF-2 treatment also increased migration and tube formation ability of EPCs even in high glucose conditions. 2) Western blot analysis demonstrated that the percentage of activated β-catenin/total β-catenin in the high glucose group were significantly lower than that in the control group, while FGF-2 treatment reversed high glucose induced β-catenin inhibition. 3) In vivo experiments demonstrated that the blood flow recovery in ischemic hind limbs of mice was significantly improved after FGF-2 treatment. Conclusion: Exogenous FGF-2 could play a role in the functional repair of damaged EPC exposed to high glucose conditions, via the activation of the Wnt/β-catenin signaling pathway. 展开更多
关键词 FIBROBLAST growth factor-2 endothelial PROGENITOR cells angiogenesis WNT/Β-CATENIN signaling pathway high glucose environment
maturity of associating liver partition and portal vein ligation for staged hepatectomy-derived liver regeneration in a rat model 预览
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作者 Yi-fan Tong Ning Meng +6 位作者 Miao-qin Chen Han-ning Ying Ming Xu Billy Lu Jun-Jie Hong Yi-fan Wang Xiujun Cai 《世界胃肠病学杂志:英文版》 SCIE CAS 2018年第10期1107-1119,共13页
AIM To establish a rat model for evaluating the maturity of liver regeneration derived from associating liver partition and portal vein ligation for staged hepatectomy(ALPPS).METHODS In the present study,ALPPS,partial... AIM To establish a rat model for evaluating the maturity of liver regeneration derived from associating liver partition and portal vein ligation for staged hepatectomy(ALPPS).METHODS In the present study,ALPPS,partial hepatecotmy(PHx),and sham rat models were established initially,which were validated by significant increase of proliferative markers including Ki-67,proliferating cell nuclear antigen,and cyclin D1.In the setting of accelerated proliferation in volume at the second and fifth day after ALPPS,the characteristics of newborn hepatocytes,as well as specific markers of progenitor hepatic cell,were identified.Afterwards,the detection of liver function followed by cluster analysis of functional gene expression were performed to evaluate the maturity.RESULTS Compared with PHx and sham groups,the proliferation of FLR was significantly higher in ALPPS group(p=0.023 and 0.001 at second day,p=0.034 and p<0.001 at fifth day after stage I).Meanwhile,the increased expression of proliferative markers including Ki-67,proliferating cell nuclear antigen,and cyclin D1 verified the accelerated liver regeneration derived from ALPPS procedure.However,ALPPS-induced Sox9 positive hepatocytes significantly increased beyond the portal triad,which indicated the progenitor hepatic cell was potentially involved.And the characteristics of ALPPSinduced hepatocytes indicated the lower expression of hepatocyte nuclear factor 4 and anti-tryptase in early proliferative stage.Both suggested the immaturity of ALPPS-derived liver regeneration.Additionally,the detection of liver function and functional genes expression confirmed the immaturity of renascent hepatocytes derived in early stage of ALPPS-derived liver regeneration.CONCLUSION Our study revealed the immaturity of ALPPS-derived proliferation in early regenerative response,which indicated that the volumetric assessment overestimated the functional proliferation.This could be convincing evidence that the stageⅡof ALPPS should be performed prudently in patients with marginally ade 展开更多
关键词 associating LIVER PARTITION and portal vein LIGATION for staged HEPATECTOMY LIVER regeneration Hepatic PROGENITOR cell Function IMMATURE
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Transplantation of bone marrow-derived endothelial progenitor cells and hepatocyte stem cells from liver fibrosis rats ameliorates liver fibrosis 预览
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作者 Ling Lan Ran Liu +5 位作者 Ling-Yun Qin Peng Cheng Bo-Wei Liu Bing-Yong Zhang Song-Ze Ding Xiu-Ling Li 《世界胃肠病学杂志:英文版》 SCIE CAS 2018年第2期237-247,共11页
AIM To explore the effectiveness for treating liver fibrosis by combined transplantation of bone marrow-derived endothelial progenitor cells(BM-EPCs)and bone marrow-derived hepatocyte stem cells(BDHSCs)from the liver ... AIM To explore the effectiveness for treating liver fibrosis by combined transplantation of bone marrow-derived endothelial progenitor cells(BM-EPCs)and bone marrow-derived hepatocyte stem cells(BDHSCs)from the liver fibrosis environment.METHODS The liver fibrosis rat models were induced with carbon tetrachloride injections for 6 wk.BM-EPCs from rats with liver fibrosis were obtained by different rates of adherence and culture induction.BDHSCs from rats with liver fibrosis were isolated by magnetic bead cell sorting.Tracing analysis was conducted by labeling EPCs with PKH26 in vitro to show EPC location in the liver.Finally,BM-EPCs and/or BDHSCs transplantation into rats with liver fibrosis were performed to evaluate the effectiveness of BM-EPCs and/or BDHSCs on liver fibrosis.RESULTS Normal functional BM-EPCs from liver fibrosis rats were successfully obtained.The co-expression level of CD133 and VEGFR2 was 63.9%±2.15%.Transplanted BM-EPCs were located primarily in/near hepatic sinusoids.The combined transplantation of BM-EPCs and BDHSCs promoted hepatic neovascularization,liver regeneration and liver function,and decreased collagen formation and liver fibrosis degree.The VEGF levels were increased in the BM-EPCs(707.10±54.32)and BM-EPCs/BDHSCs group(615.42±42.96),compared with those in the model group and BDHSCs group(P<0.05).Combination of BM-EPCs/BDHSCs transplantation induced maximal up-regulation of PCNA protein and HGF mRNA levels.The levels of alanine aminotransferase(AST),aspartate aminotransferase,total bilirubin(TBIL),prothrombin time(PT)and activated partial thromboplastin time in the BMEPCs/BDHSCs group were significantly improved,to be equivalent to normal levels(P>0.05)compared with those in the BDHSC(AST,TBIL and PT,P<0.05)and BM-EPCs(TBIL and PT,P<0.05)groups.Transplantation of BM-EPCs/BDHSCs combination significantly reduced the degree of liver fibrosis(staging score of 1.75±0.25 vs BDHSCs 2.88±0.23 or BMEPCs 2.75±0.16,P<0.05).CONCLUSION The combined transplantation exhibited maximal thera 展开更多
关键词 Bone marrow Endothelial PROGENITOR cells LIVER stem CELL CELL TRANSPLANTATION LIVER fibrosis
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Yiguanjian decoction enhances fetal liver stem/progenitor cell-mediated repair of liver cirrhosis through regulation of macrophage activation state 预览
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作者 Ying Xu Wei-Wei Fan +7 位作者 Wen Xu Shi-Li Jiang Gao-Feng Chen Cheng Liu Jia-Mei Chen Hua Zhang Ping Liu Yong-Ping Mu 《世界胃肠病学杂志:英文版》 SCIE CAS 2018年第42期4759-4772,共14页
AIM To investigate whether Yiguanjian decoction(YGJ)has an anti-liver cirrhotic effect and whether it regulates hepatic stem cell differentiation.METHODS A rat model of liver cirrhosis was established via subcutaneous... AIM To investigate whether Yiguanjian decoction(YGJ)has an anti-liver cirrhotic effect and whether it regulates hepatic stem cell differentiation.METHODS A rat model of liver cirrhosis was established via subcutaneous injection of carbon tetrachloride(CCl4)for 8 wk.From the beginning of the ninth week,the rats received 2-acetylaminofluorene(2-AAF)by oral gavage and a DLK-1+fetal liver stem/progenitor cell(FLSPC)transplant or an FLSPC transplant in combination with YGJ treatment for 4 wk.In vitro,lipopolysaccharide(LPS)-activated macrophages were co-cultured with WB-F344 cells,and the differentiation of WB-F344 cells was observed in the presence and absence of YGJ treatment.RESULTS FLSPC transplantation improved liver function and histopathology,and inhibited the activation of the noncanonical Wnt signaling pathway,while activating the canonical Wnt signaling pathway.YGJ enhanced the therapeutic effects of FLSPCs and also promoted the liver regeneration differentiation of FLSPCs into hepatocytes.In vitro,LPS-activated macrophages promoted the differentiation of WB-F344 cells into myofibroblasts,and the canonical Wnt signaling was inhibited while the noncanonical Wnt signaling was activated in WB-F344 cells.YGJ suppressed the activation of macrophages and then inhibited non-canonical Wnt signaling and promoted canonical Wnt signaling.CONCLUSION YGJ enhances FLSPC-mediated repair of liver cirrhosis through regulation of macrophage activation state,and YGJ in combination with stem cell transplantation may be a suitable treatment for end-stage liver cirrhosis. 展开更多
关键词 CIRRHOSIS Hepatic PROGENITOR cells Wnt signaling pathway MACROPHAGE 2-acetylaminofluorene Carbon TETRACHLORIDE Yiguanjian DECOCTION
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CD29的表达与人类唾液腺良恶性肿瘤发病关系的研究 预览
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作者 刘鑫灿 张德保 刘仔龙 《口腔医学研究》 北大核心 2018年第11期1204-1207,共4页
目的:分析与明确各种细胞表面标记物的表达和分布,特别是CD29在成人唾液腺中的表达和分布。方法:采集成对的成人腮腺、舌下腺和颌下腺组织。并使用免疫组化检测收集的腺体中各种家族特异性细胞表面标记的表型表达(包括CD29)。结果:发现C... 目的:分析与明确各种细胞表面标记物的表达和分布,特别是CD29在成人唾液腺中的表达和分布。方法:采集成对的成人腮腺、舌下腺和颌下腺组织。并使用免疫组化检测收集的腺体中各种家族特异性细胞表面标记的表型表达(包括CD29)。结果:发现CD29在唾液腺腺泡和导管上皮,间充质基质和肌上皮细胞上均有表达;CD29+细胞在成人唾液腺上皮中与CD324、CD326、NKCC1和CD44共表达;间充质细胞主要表达CD73、CD90、波形蛋白和CD34而α-SMA主要是肌上皮细胞特异性祖细胞标记物。结论:CD29广泛表达于人唾液腺中,可作为唾液腺疾病和恶性肿瘤新型细胞治疗和诊断的潜在生物标志物。 展开更多
关键词 成人 CD 29 祖细胞 唾液腺 干细胞
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Regulatory role of sphingosine kinase and sphingosine-1-phosphate receptor signaling in progenitor/stem cells 预览
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作者 Mei Li Ng Nagendra S Yarla +1 位作者 Mario Menschikowski Olga A Sukocheva 《世界干细胞杂志:英文版(电子版)》 2018年第9期119-133,共15页
Balanced sphingolipid signaling is important for the maintenance of homeostasis.Sphingolipids were demonstrated to function as structural components,second messengers,and regulators of cell growth and survival in norm... Balanced sphingolipid signaling is important for the maintenance of homeostasis.Sphingolipids were demonstrated to function as structural components,second messengers,and regulators of cell growth and survival in normal and disease-affected tissues.Particularly,sphingosine kinase 1(SphK1)and its product sphingosine-1-phosphate(S1P)operate as mediators and facilitators of proliferation-linked signaling.Unlimited proliferation(selfrenewal)within the regulated environment is a hallmark of progenitor/stem cells that was recently associated with the S1P signaling network in vasculature,nervous,muscular,and immune systems.S1P was shown to regulate progenitor-related characteristics in normal and cancer stem cells(CSCs)via G-protein coupled receptors S1Pn(n=1 to 5).The SphK/S1P axis is crucially involved in the regulation of embryonic development of vasculature and the nervous system,hematopoietic stem cell migration,regeneration of skeletal muscle,and development of multiple sclerosis.The ratio of the S1P receptor expression,localization,and specific S1P receptoractivated downstream effectors influenced the rate of selfrenewal and should be further explored as regenerationrelated targets.Considering malignant transformation,it is essential to control the level of self-renewal capacity.Proliferation of the progenitor cell should be synchronized with differentiation to provide healthy lifelong function of blood,immune systems,and replacement of damaged or dead cells.The differentiation-related role of SphK/S1P remains poorly assessed.A few pioneering investigations explored pharmacological tools that target sphingolipid signaling and can potentially confine and direct self-renewal towards normal differentiation.Further investigation is required to test the role of the SphK/S1P axis in regulation of self-renewal and differentiation. 展开更多
关键词 Sphingosine-1-phosphate SPHINGOLIPIDS Embryonic STEM CELLS Mesenchymal STEM CELLS Bone marrow hematopoietic STEM CELLS SPHINGOSINE kinase PROGENITOR
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胶质细胞干细胞/前体细胞特性的研究进展 被引量:1
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作者 谭子健 巨淑慧 +2 位作者 黄潇 谷亚坤 苏志达 《生理学报》 CAS CSCD 北大核心 2017年第2期207-217,共11页
胶质细胞是脑内数量最多的神经细胞,包括星形胶质细胞、少突胶质前体细胞、NG2胶质细胞等多种类型,具有维持神经系统内环境稳态、支持和营养神经元、调控神经信号传导等多种重要功能。近年来,随着研究的深入,越来越多的证据表明某... 胶质细胞是脑内数量最多的神经细胞,包括星形胶质细胞、少突胶质前体细胞、NG2胶质细胞等多种类型,具有维持神经系统内环境稳态、支持和营养神经元、调控神经信号传导等多种重要功能。近年来,随着研究的深入,越来越多的证据表明某些特定的胶质细胞在一定条件下表现出干细胞的特性,发挥干细胞的功能。例如,在病理损伤条件下,星形胶质细胞和少突胶质前体细胞均会被活化而出现增殖、分化,体外分离培养可自我更新形成神经球。这些活化的星形胶质细胞和少突胶质前体细胞形成的神经球能够被诱导分化为星形胶质细胞、少突胶质细胞和神经元。此外,通过强制性表达外源基因能将星形胶质细胞和NG2胶质细胞转分化为神经元,这可能也是其干细胞特性的一种体现。本文在已有研究的基础上,总结了放射状胶质细胞、少突胶质前体细胞、星形胶质细胞、NG2胶质细胞与其它类型胶质细胞的干细胞特性、干细胞特性形成的条件、它们可能产生的子代细胞以及涉及的分子信号调控通路。深入探讨胶质细胞的干细胞特性及生理功能,有利于促进其在神经系统损伤修复领域的临床应用。 展开更多
关键词 胶质细胞 神经干细胞 前体细胞 生物学特性 功能
PDK1对中性粒细胞分化的影响 预览
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作者 王伟丽 王乐 +2 位作者 胡甜园 李聪 袁卫平 《中国实验血液学杂志》 CSCD 北大核心 2017年第3期932-935,共4页
目的:应用Vav-Cre在成体小鼠敲除PDK1并观察PDK1敲除对中性粒细胞比例、数目及分化的影响。方法:应用RT-PCR分析PDK1敲除后骨髓细胞PDK1表达水平;应用CFU-C实验检测PDK1对祖细胞功能的影响;应用流式细胞术分析PDK1对中性粒细胞比例的... 目的:应用Vav-Cre在成体小鼠敲除PDK1并观察PDK1敲除对中性粒细胞比例、数目及分化的影响。方法:应用RT-PCR分析PDK1敲除后骨髓细胞PDK1表达水平;应用CFU-C实验检测PDK1对祖细胞功能的影响;应用流式细胞术分析PDK1对中性粒细胞比例的影响。结果:PDK1敲除后骨髓细胞PDK1表达水平很低;粒系祖细胞及巨噬祖细胞数目减少;中性粒细胞比例数目减少,但幼稚的中性粒细胞比例增多。结论:PDK1敲除影响了造血干细胞向祖细胞分化的过程,以及中性粒细胞的分化成熟过程。 展开更多
关键词 PDK1 中性粒细胞 祖细胞
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