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| 1 | Angiogenesis and neuronal remodeling after ischemic stroke显示文摘Increased microvessel density in the peri-infarct region has been reported and has been correlated with longer survival times in ischemic stroke patients and has improved outcomes in ischemic animal models.This raises the possibility that enhancement of angiogenesis is one of the strategies to facilitate functional recovery after ischemic stroke.Blood vessels and neuronal cells communicate with each other using various mediators and contribute to the pathophysiology of cerebral ischemia as a unit.In this mini-review,we discuss how angiogenesis might couple with axonal outgrowth/neurogenesis and work for functional recovery after cerebral ischemia.Angiogenesis occurs within 4 to 7 days after cerebral ischemia in the border of the ischemic core and periphery.Post-ischemic angiogenesis may contribute to neuronal remodeling in at least two ways and is thought to contribute to functional recovery.First,new blood vessels that are formed after ischemia are thought to have a role in the guidance of sprouting axons by vascular endothelial growth factor and laminin/β1-integrin signaling.Second,blood vessels are thought to enhance neurogenesis in three stages:1)Blood vessels enhance proliferation of neural stem/progenitor cells by expression of several extracellular signals,2)microvessels support the migration of neural stem/progenitor cells toward the peri-infarct region by supplying oxygen,nutrients,and soluble factors as well as serving as a scaffold for migration,and 3)oxygenation induced by angiogenesis in the ischemic core is thought to facilitate the differentiation of migrated neural stem/progenitor cells into mature neurons.Thus,the regions of angiogenesis and surrounding tissue may be coupled,representing novel treatment targets. | Masahiro Hatakeyama Itaru Ninomiya Masato Kanazawa | 2020 | Neural Regeneration Research2020，15，1： | 63 |
| 2 | Effects of salvianolic acid B on proliferation, neurite outgrowth and differentiation of neural stem cells derived from the cerebral cortex of embryonic mice显示文摘Salvianolic acid B is isolated from Salvia miltiorrhiza,the root of which is widely used as a traditional Chinese medicine to treat stroke.However,little is known about how salvianolic acid B influences growth characteristics of neural stem cells (NSCs).The purpose of the present study was to evaluate the effects of salvianolic acid B on proliferation,neurite outgrowth and differentiation of NSCs derived from the cerebral cortex of embryonic mice using MTT,flow cytometry,immunofluorescence and RT-PCR.It was found that 20 μg mL·1 and 40 μg mL·1 salvianolic acid B had similar effects on proliferation of NSCs,and a suitable concentration of salvianolic acid B increased the number of NSCs and their derivative neurospheres.The growth-promoting activity of salvianolic acid B was dependent on and associated with an accumulation in the G2/S-phase cell population.Salvianolic acid B also promoted the neurite outgrowth of NSCs and their differentiation into neurons.The mRNA for tau,GFAP and nestin were present in differentiating neurospheres induced by salvianolic acid B.However,high-level expression of tau mRNA and low-level expression of GFAP mRNA was detected in differentiated cells,in contrast to the control conditions.This collective evidence indicates that exogenous salvianolic acid B is capable of promoting proliferation of neurospheres and differentiation towards the neuronal lineage in vitro and may act in the proliferation of NSCs and may promote NSC differentiation into neuronal cells. | GUO GuoQing1,LI Bin1,WANG YuanYuan1,SHAN AiJing1,SHEN WeiZai1,YUAN Lin2 & ZHONG ShiZhen2 1Department of Anatomy,Medical College of Jinan University,Guangzhou 510630,China 2Institute of Clinical Anatomy,Key Laboratory of Tissue Construction and Detection of Guangdong Province,Southern Medical University,Guangzhou 510150,China | 2010 | Science China(Life Sciences)2010，53，6： | 21 |
| 3 | Pleiotrophin promotes perineural invasion in pancreatic cancer显示文摘Perineural invasion(PNI)in pancreatic cancer is an important cause of local recurrence,but little is known about its mechanism.Pleiotrophin(PTN)is an important neurotrophic factor.It is of interest that our recent experimental data showed its involvement in PNI of pancreatic cancer.PTN strongly presents in the cytoplasm of pancreatic cancer cells,and high expression of PTN and its receptor may contribute to the high PNI of pancreatic cancer.Correspondingly,PNI is prone to happen in PTN-positive tumors.We thus hypothesize that,as a neurite growth-promoting factor,PTN may promote PNI in pancreatic cancer.PTN is released at the time of tumor cell necrosis,and binds with its highaffinity receptor,N-syndecan on pancreatic nerves,to promote neural growth in pancreatic cancer.Furthermore,neural destruction leads to a distorted neural homeostasis.Neurons and Schwann cells produce more N-syndecan in an effort to repair the pancreatic nerves.However,the abundance of N-syndecan attracts further PTN-positive cancer cells to the site of injury,creating a vicious cycle.Ultimately,increased PTN and N-syndecan levels,due to the continuous nerve injury,may promote cancer invasion and propagation along the neural structures.Therefore,it is meaningful to discuss the relationship between PTN/N-syndecan signaling and PNI in pancreatic cancer,which may lead to a better understanding of the mechanism of PNI in pancreatic cancer. | Jun Yao Xiu-Feng Hu Xiao-Shan Feng She-Gan Gao | 2013 | World Journal of Gastroenterology2013，19，39： | 11 |
| 4 | Outgrowth endothelial cells form a functional cerebral barrier and restore its integrity after damage显示文摘Breakdown of blood-brain barrier,formed mainly by brain microvascular endothelial cells(BMECs),represents the major cause of mortality during early phases of ischemic strokes.Hence,discovery of novel agents that can effectively replace dead or dying endothelial cells to restore blood-brain barrier integrity is of paramount importance in stroke medicine.Although endothelial progenitor cells(EPCs)represent one such agents,their rarity in peripheral blood severely limits their adequate isolation and therapeutic use for acute ischemic stroke which necessitate their ex vivo expansion and generate early EPCs and outgrowth endothelial cells(OECs)as a result.Functional analyses of these cells,in the present study,demonstrated that only OECs endocytosed DiI-labelled acetylated low-density lipoprotein and formed tubules on matrigel,prominent endothelial cell and angiogenesis markers,respectively.Further analyses by flow cytometry demonstrated that OECs expressed specific markers for sternness(CD34),immaturity(CD133)and endothelial cells(CD31)but not for hematopoietic cells(CD45).Like BMECs,OECs established an equally tight in vitro model of human BBB with astrocytes and pericytes,suggesting their capacity to form tight junctions.Ischemic injury mimicked by concurrent deprivation of oxygen and glucose(4 hours)or deprivation of oxygen and glucose followed by reperfusion(20 hours)affected both barrier integrity and function in a similar fashion as evidenced by decreases in transendothelial electrical resistance and increases in paracellular flux,respectively.Wound scratch assays comparing the vasculoreparative capacity of cells revealed that,compared to BMECs,OECs possessed a greater proliferative and directional migratory capacity.In a triple culture model of BBB established with astrocytes,pericytes and BMEC,exogenous addition of OECs effectively repaired the damage induced on endothelial layer in serum-free conditions.Taken together,these data demonstrate that OECs may effectively home to the site of vascular injury and repair the damage to maintain(neuro)vascular homeostasis during or after a cerebral ischemic injury. | Rais Reskiawan Abdulkadir Mansour Alwjwaj Othman Ahmad Othman Kamini Rakkar Ulvi Bayraktutan | 2020 | Neural Regeneration Research2020，15，6： | 5 |
| 5 | Role of miR-124 in the regulation of retinoic acid-induced Neuro-2A cell differentiation显示文摘Retinoic acid can cause many types of cells,including mouse neuroblastoma Neuro-2 A cells,to differentiate into neurons.However,it is still unknown whether microRNAs(miRNAs)play a role in this neuronal differentiation.To address this issue,real-time polymerase chain reaction assays were used to detect the expression of several differentiation-related miRNAs during the differentiation of retinoic acid-treated Neuro-2 A cells.The results revealed that miR-124 and miR-9 were upregulated,while miR-125 b was downregulated in retinoic acid-treated Neuro-2 A cells.To identify the miRNA that may play a key role,miR-124 expression was regulated by transfection of miRNA mimics or inhibitors.Morphological analysis results showed that inhibition of miR-124 expression reversed the effects of retinoic acid on neurite outgrowth.Moreover,miR-124 overexpression alone caused Neuro-2 A cells to differentiate into neurons,and its inhibitor could block this effect.These results suggest that miR-124 plays an important role in retinoic acid-induced differentiation of Neuro-2 A cells. | Qun You Qiang Gong Yu-Qiao Han Rou Pi Yi-Jie Du Su-Zhen Dong | 2020 | Neural Regeneration Research2020，15，6： | 4 |
| 6 | 急性一氧化碳中毒致迟发性脑病大鼠胼胝体损伤及神经生长抑制因子A的表达显示文摘目的:研究急性一氧化碳( carbon monoxide , CO )中毒致迟发性脑病( delayed neuropsychologic sequelae , DNS )大鼠胼胝体的损伤及神经生长抑制因子 A ( neurite outgrowth inhibitor-A, Nogo-A)的表达情况。方法腹腔内分次注射CO气体造成DNS模型,于不同时间点取胼胝体。HE染色观察细胞形态,变色酸染色观察脱髓鞘改变,免疫组化检测观察Nogo-A蛋白表达,荧光定量聚合酶链式反应( real time polymerase chain reaction , RT-PCR)检测Nogo-A mRNA表达,电镜观察胼胝体超微结构变化。结果中毒组光镜下胼胝体出现脱髓鞘等变化,以造模成功后0 h变化较明显。免疫组化显示,Nogo-A在各时间点均高表达(P<0.05)。 RT-PCR于造模成功后0、12、24 h高表达(P<0.05),0 h为高峰,其后逐渐下降,第3天与对照组比较差异无统计学意义,中毒组第7天表达再次升高(P<0.05)。电镜下,胼胝体出现相应改变。结论 CO中毒后大鼠胼胝体出现脱髓鞘损伤,且与Nogo-A表达相关。 | 杨允 王新春 李林 陆莹 | 2014 | 中国急救医学2014，34，8： | 2 |
| 7 | GPR3,GPR6,and GPR12 as novel molecular targets:their biological functions and interaction with cannabidiol显示文摘The G protein-coupled receptors 3,6,and 12(GPR3,GPR6,and GPR12)comprise a family of closely related orphan receptors with no con firmed en dogenous liga nds.These receptors are con stitutively active and capable of signaling through G protein-mediated and non-G protein-mediated mechanisms.These orphan receptors have previously been reported to play important roles in many normal physiological functions and to be involved in a variety of pathological conditions.Although they are orphans,GPR3,GPR6,and GPR12 are phylogenetically most closely related to the cannabinoid receptors.Using β-arrestin2 recruitment and cAMP accumulati on assays,we recently found that the non psychoactive phytoca nnabinoid cann abidiol(CBD)is an inverse agonist for GPR3,GPR6,and GPR12.This discovery highlights these orphan receptors as potential new molecular targets for CBD,provides novel mechanisms of action,and suggests new therapeutic uses of CBD for illnesses such as Alzheimer's disease,Parkinson's disease,can cer,and infertility.Furthermore,identificati on of CBD as a new in verse agonist for GPR3,GPR6,and GPR12 provides the initial chemical scaffolds upon which potent and efficacious agents acting on these receptors can be developed,with the goal of developing chemical tools for studying these orphan receptors and ultimately new therapeutic agents. | Alyssa S.Laun Sarah H.Shrader Kevin J.Brown Zhao-Hui Song | 2019 | Acta Pharmacologica Sinica2019，40，3： | 2 |
| 8 | Safflower Yellow Compounds Alleviate Okadaic Acid-Induced Impairment of Neurite Outgrowth in Differentiated SH-SY5Y Cells显示文摘The dynamic assembly of microtubules plays a key role in maintaining structural and functional integrity of eukaryotic cel s,especial y with regard to neuronal differentiation or neurite outgrowth and synaptic plasticity,which contribute to the development of the nervous system and memory formation. | WANG Zhen Hua SHI Xiao Bing LI Gang HAO Xue Yan YUAN Zhen Zhen CAO Xiao Hai WANG Hong Lun LI Ji MA Cheng Jun | 2020 | Biomedical and Environmental Sciences2020，33，10： | 1 |
| 9 | Distinct functions of Trio GEF domains in axon outgrowth of cerebellar granule neurons显示文摘As a critical guanine nucleotide exchange factor(GEF) regulating neurite outgrowth, Trio coordinates multiple processes of cytoskeletal dynamics through activating Rac1, Cdc42 and RhoA small GTPases by two GEF domains, but the in vivo roles of these GEF domains and corresponding downstream effectors have not been determined yet. We established multiple lines of knockout mice and assessed the respective roles of Trio GEF domains and Rac1 in axon outgrowth. Knockout of total Trio in cerebellar granule neurons(CGNs) led to an impaired F-actin rearrangement of growth cone and hence a retarded neurite outgrowth. Such a retardation was reproduced by inhibition of GEF1 domain or knockdown of Cdc42 and restored apparently by introduction of active Cdc42. As Rac1 deficiency did not affect the neurite outgrowth of CGNs, we suggested that Trio GEF1-mediated Cdc42 activation was required for neurite outgrowth. We established a GEF2-knockout line with deletion of all Trio isoforms except a cerebella-specific Trio8, a short isoform of Trio without GEF2 domain, and used this line as a GEF2-deficient animal model. The GEF2-deficient CGNs had a normal neurite outgrowth but abolished Netrin-1-promoted growth, without affecting Netrin-1 induced Rac1 activation. We thus suggested that Trio GEF1-mediated Cdc42 activation rather than Rac1 activation drives the F-actin dynamics necessary for neurite outgrowth, while GEF2 functions in Netrin-1-promoted neurite elongation. Our results delineated the distinct roles of Trio GEF domains in neurite outgrowth, which is instructive to understand the pathogenesis of clinical Trio-related neurodevelopmental disorders. | Tao Tao Jie Sun Yajing Peng Pei Wang Xin Chen Wei Zhao Yeqiong Li Lisha Wei Wei Wang Yanyan Zheng Ye Wang Xuena Zhang Min-Sheng Zhu | 2019 | Journal of Genetics and Genomics2019，46，2： | 1 |
| 10 | The effects of human genome DNA on spinal cord neurons of the embryonic mouse in vitro显示文摘objective: To study the effects of human genome DNA on the cultured spinal cord neurons of em bryonic mouse. Methods: The human genome DNA was added to the culture medium of the spinal cord neu rons of embryonic mouse. Eight days later, MTT assay, NSE immunocytochemical staining and image analy sis were proformed to examine the viabilities and the neurites lengths of the neurons. Results: The neurite length of the experimental group was significantly Ionger than that of the control group, but no marked dif ference was found between the viabilities of the neurons of the experimental groups and that of the control ones. Conclusiou: Human genome DNA has no effects on the viabilities of the cultured neurons but can pro mote the neurite growth. | 杨大莉 梁喆 鞠躬 | 1999 | Journal of Medical Colleges of PLA(China)1999，14，3： | 0 |
| 11 | The role of cell surface β1, 4-galactosyltransferase duringectoplacentacone outgrowth on laminin显示文摘Theroleofcellsurfaceβ1,4-galactosyltransferaseduringectoplacentaconeoutgrowth on lamininZhangChunyu(张春雨),CaoYujing(曹宇靖),DuanE... | 张春雨 段恩奎 曹宇靖 曾国庆 张春雨 曹宇靖 段恩奎 曾国庆 | 1996 | 生殖医学杂志1996，5，S1： | 0 |
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