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Chinese Medicine’s Intervention Effect on Nogo-A/NgR
Xiu-de Qin,Li-yuan Kang,Yu Liu,Yan Huang,Shuo Wang,Jin-qiang Zhu
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/528482
Abstract: Cerebral vascular disease is very common in the elderly and is one of the most dangerous diseases which is hazardous to the body’s health, and it is the medical specialists’ study hot spot not only in the clinical field but also in the medical basic research field. Neural regeneration has been paid more and more attention in recent years. Nogo’s function in the process of neural regeneration has become the focal point since it was discovered in the year 2000. Many studies elucidate that Nogo negatively affects the neural regeneration and plasticity. Chinese medicine plays an important role in the prevention and treatment of neural diseases, and recently some researches about the Chinese medicine’s intervention effect on Nogo-A/NgR sprang up, so it is necessary to make a review on this aspect.
Nogo-Receptors NgR1 and NgR2 Do Not Mediate Regulation of CD4 T Helper Responses and CNS Repair in Experimental Autoimmune Encephalomyelitis  [PDF]
Karin Steinbach, Claire L. McDonald, Markus Reindl, Rüdiger Schweigreiter, Christine Bandtlow, Roland Martin
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026341
Abstract: Myelin-associated inhibition of axonal regrowth after injury is considered one important factor that contributes to regeneration failure in the adult central nervous system (CNS). Blocking strategies targeting this pathway have been successfully applied in several nerve injury models, including experimental autoimmune encephalomyelitis (EAE), suggesting myelin-associated inhibitors (MAIs) and functionally related molecules as targets to enhance regeneration in multiple sclerosis. NgR1 and NgR2 were identified as interaction partners for the myelin proteins Nogo-A, MAG and OMgp and are probably mediating their growth-inhibitory effects on axons, although the in vivo relevance of this pathway is currently under debate. Recently, alternative functions of MAIs and NgRs in the regulation of immune cell migration and T cell differentiation have been described. Whether and to what extent NgR1 and NgR2 are contributing to Nogo and MAG-related inhibition of neuroregeneration or immunomodulation during EAE is currently unknown. Here we show that genetic deletion of both receptors does not promote functional recovery during EAE and that NgR1 and NgR2-mediated signals play a minor role in the development of CNS inflammation. Induction of EAE in Ngr1/2-double mutant mice resulted in indifferent disease course and tissue damage when compared to WT controls. Further, the development of encephalitogenic CD4+ Th1 and Th17 responses was unchanged. However, we observed a slightly increased leukocyte infiltration into the CNS in the absence of NgR1 and NgR2, indicating that NgRs might be involved in the regulation of immune cell migration in the CNS. Our study demonstrates the urgent need for a more detailed knowledge on the multifunctional roles of ligands and receptors involved in CNS regeneration failure.
电针对局灶性脑梗死大鼠Nogo-A及其受体NgR和运动诱发电位的影响  [PDF]
第三军医大学学报 , 2013,
Abstract: 目的观察电针对局灶性脑梗死大鼠运动诱发电位和梗死周围组织神经抑制因子Nogo-A及其受体NgR等的影响,探讨电针治疗脑梗死的机制。方法将36只成年SD大鼠,分为正常对照组、模型组和电针组(每组12只)。电针组和模型组按照改进后的Longa的方法制作大脑中动脉闭塞模型。正常组和模型组不做任何治疗,电针组在造模成功后第1天进行电针治疗。3组均在造模后1d和14d进行运动诱发电位(MEP)检测,14d时进行HE染色和Nissl染色观察大鼠脑组织病理变化,免疫组化染色和Westernblot法检测Nogo-A和NgR在脑组织内的表达。结果14d时,电针组MEPN1波的潜伏期(15.38±1.58)ms和N2波的潜伏期(33.60±3.58)ms较模型组N1波的潜伏期(21.28±4.00)ms和N2波的潜伏期(41.78±3.07)ms明显好转(P<0.01);HE染色结果显示,电针组脑组织较模型组梗死区域的神经细胞病变程度明显改善;Nissl染色结果显示,电针组的Nissl小体数目较模型组增多,肿胀的神经细胞内可见Nissl小体分布;免疫组化检测结果显示,电针组的Nogo-A和NgR的表达较模型组明显减少(P<0.05,P<0.01);Westernblot检测结果显示,电针组Nogo-A蛋白(22.45±0.95)%和NgR蛋白(26.76±1.14)%较模型组[Nogo-A蛋白(43.75±6.21)%,NgR蛋白(54.50±5.00)%]明显减少(P<0.01)。结论电针能明显改善急性脑梗死大鼠的神经传导通路,改善梗死区组织病理表现,减少Nogo-A和NgR在脑组织内的表达,促进神经功能缺失症状的恢复。
Differential Conserted Activity Induced Regulation of Nogo Receptors (1–3), LOTUS and Nogo mRNA in Mouse Brain  [PDF]
Tobias E. Karlsson, Josefin Koczy, Stefan Brené, Lars Olson, Anna Josephson
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060892
Abstract: Nogo Receptor 1 (NgR1) mRNA is downregulated in hippocampal and cortical regions by increased neuronal activity such as a kainic acid challenge or by exposing rats to running wheels. Plastic changes in cerebral cortex in response to loss of specific sensory inputs caused by spinal cord injury are also associated with downregulation of NgR1 mRNA. Here we investigate the possible regulation by neuronal activity of the homologous receptors NgR2 and NgR3 as well as the endogenous NgR1 antagonist LOTUS and the ligand Nogo. The investigated genes respond to kainic acid by gene-specific, concerted alterations of transcript levels, suggesting a role in the regulation of synaptic plasticity, Downregulation of NgR1, coupled to upregulation of the NgR1 antagonist LOTUS, paired with upregulation of NgR2 and 3 in the dentate gyrus suggest a temporary decrease of Nogo/OMgp sensitivity while CSPG and MAG sensitivity could remain. It is suggested that these activity-synchronized temporary alterations may serve to allow structural alterations at the level of local synaptic circuitry in gray matter, while maintaining white matter pathways and that subsequent upregulation of Nogo-A and NgR1 transcript levels signals the end of such a temporarily opened window of plasticity.
Localisation and Expression of a Myelin Associated Neurite Inhibitor, Nogo-A and its Receptor Nogo-Receptor by Mammalian CNS Cells
E. Nyatia,D.M. Lang
International Journal of Molecular Medicine and Advance Sciences , 2011,
Abstract: Axon regeneration failure in the adult mammalian Central Nervous System (CNS) is partly due to inhibitory molecules associated with myelin. The Nogo receptor (NgR) plays a role in this process through an extraordinary degree of cross reactivity with three structurally unrelated myelin-associated inhibitory ligands namely; Nogo-A, Myelin Associated Glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp). The major aim of the study was to investigate and explore the cellular localisation and expression pattern of NgR and Nogo-A in the mammalian nervous system. We therefore generated a rabbit polyclonal anti-NgR antibody from the leucine rich repeat (LRR) No. 9 domain of the NgR polypeptide chain. Together with a commercially available polyclonal antibody specific for NgR and in conjunction with double labeling immunofluorescence methods on cryosections and cell cultures, NgR immunoreactivity was observed in the CNS and Dorsal Root Ganglia (DRG). In cellular populations, it was confined to neuronal cell bodies and their processes. NgR was also localised on the surface of extending DRG intact axons and growth cones in live staining experiments. Nogo-A, a member of the reticulon family protein, was widely distributed in the mammalian brain, spinal cord and DRG. Intense Nogo-A immunoreactivity was also detected in oligodendrocyte cell bodies and their myelin sheaths in nerve fibre tracts of the CNS. Furthermore, numerous populations of neurons in the brain and spinal cord expressed Nogo-A to a variable extent in their cell bodies and neurites, suggesting additional, as-yet-unknown, functions of this protein. These results confirm results obtained by other researchers with different sets of antibodies. However, they also raise the question of the mechanism and circumstances under which NgR interacts with Nogo-A, as the latter appears to be confined to the cytoplasm and can therefore not be expected to bind NgR on the axon surface.
Nogo receptor is involved in the adhesion of dendritic cells to myelin
Claire L McDonald, Karin Steinbach, Florian Kern, Rüdiger Schweigreiter, Roland Martin, Christine E Bandtlow, Markus Reindl
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-113
Abstract: Human DCs were differentiated from peripheral blood monocytes and mouse DCs were differentiated from wild type and NgR1/NgR2 double knockout bone marrow precursors. NgR1 and NgR2 expression were determined with quantitative real time PCR and immunoblot, and adhesion of cells to myelin was quantified.We demonstrate that human immature myeloid DCs express NgR1 and NgR2, which are then down-regulated upon maturation. Human mature DCs also adhere to a much higher extent to a myelin substrate than immature DCs. We observe the same effect when the cells are plated on Nogo-66-His (binding peptide for NgR1), but not on control proteins. Mature DCs taken from Ngr1/2 knockout mice adhere to a much higher extent to myelin compared to wild type mouse DCs. In addition, Ngr1/2 knockout had no effect on in vitro DC differentiation or phenotype.These results indicate that a lack of NgR1/2 expression promotes the adhesion of DCs to myelin. This interaction could be important in neuroinflammatory disorders such as multiple sclerosis in which peripheral immune cells come into contact with myelin debris.Injury to the central nervous system (CNS) has long been known to cause fatal and irreversible damage to axons and neurons. A number of physical and molecular inhibitory factors expressed by neurons, astrocytes, and oligodendrocytes serve to maintain the architecture of the mature CNS, but at the same time contribute to the lack of repair mechanisms following damage. Some of the major molecular inhibitors to regeneration are those associated with myelin (myelin-associated inhibitory factors, MAIFs). MAIFs include Nogo-A [1,2], myelin-associated glycoprotein (MAG) [3,4] and oligodendrocyte-myelin glycoprotein (OMgp) [5]. These factors are all binding partners for the Nogo-66 receptor-1 (NgR1), a mainly neuron-expressed, GPI-anchored protein [6-8]. Nogo-66 is a 66 amino acid long region of Nogo-A that binds NgR1 and is largely responsible for inhibiting neurite outgrowth. Since the identi
《神乌傅(赋)》用经、子文谫论  [PDF]
东南文化 , 2009,
Abstract: ????《神乌傅(赋)》或引用、或化用《诗经》、《论语》、《周易》、《孝经》、《老子》、《庄子》、《荀子》等典籍,文字与今传本多有差异。以《神乌傅(赋)》考论典籍,可补通行典籍之缺,增《诗三家义集疏》中《齐诗》说内容;以典籍释读《神乌傅(赋)》可明作者习《齐诗》、谙《论语》,初步释读“止于樊”、“?自”、“去色就安”、“不意不信”等词,裨益文本解读,以更好地理解《神乌傅(赋)》文意。据此,结合西汉官学教育体制,我们对赋作者习学和受教的情况有了个大致臆测。
Nogo-66受体RNA干扰质粒的构建及其干扰效率鉴定  [PDF]
第三军医大学学报 , 2007,
Abstract: 目的构建及筛选高效率针对Nogo-66受体(Nogo-66receptor,NgR)进行RNA干扰(RNAi)的质粒。方法RT-PCR克隆NgR,插入表达质粒中,构建NgR-GFP融合蛋白表达质粒。根据NgR序列,设计4对针对NgRmRNA进行RNAi的寡核苷酸。退火后,插入短发夹RNA(shorthairpinRNA,shRNA)表达质粒中,构建shRNA表达质粒。将NgR-GFP融合蛋白表达质粒与shRNA表达质粒共转染AAV-293细胞。通过对GFP表达量的观察及Westernblotting定量检测NgR-GFP融合蛋白表达量,鉴定shRNA表达质粒对NgR的干扰效率。结果针对NgR进行RNAi的4个序列中,有1个序列的干扰效率大于90%以上。结论成功构建了1个针对NgR的高效RNAi表达质粒。
nogo与nogo受体研究  [PDF]
生物化学与生物物理进展 , 2002,
Abstract: nogo是新近发现的一种基因,编码3种蛋白质:nogo-a、nogo-b和nogo-c.迄今为止,已证明它有抑制成熟中枢神经系统(cns)神经元轴突再生及诱导细胞凋亡的作用.nogo受体是一种糖基醇磷脂结合蛋白.对nogo和nogo受体的研究,对于cns再生障碍及肿瘤的认识和治疗有重要意义.
Inhibitory Activity of Myelin-Associated Glycoprotein on Sensory Neurons Is Largely Independent of NgR1 and NgR2 and Resides within Ig-Like Domains 4 and 5  [PDF]
Verena W?rter, Rüdiger Schweigreiter, Bernd Kinzel, Matthias Mueller, Carmen Barske, Günther B?ck, Stefan Frentzel, Christine E. Bandtlow
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005218
Abstract: Myelin-associated glycoprotein (MAG) is a sialic acid binding Ig-like lectin (Siglec) which has been characterized as potent myelin-derived inhibitor of neurite outgrowth. Two members of the Nogo-receptor (NgR) family, NgR1 and NgR2, have been identified as neuronal binding proteins of MAG. In addition, gangliosides have been proposed to bind to and confer the inhibitory activity of MAG on neurons. In this study, we investigated the individual contribution of NgRs and gangliosides to MAG-mediated inhibition of sensory neurons derived from dorsal root ganglia (DRG) of ngr1, ngr2 or ngr1/ngr2 deletion mutants. We found no disinhibition of neurite growth in the absence of either NgR1 or NgR2. Sensory neurons deficient for both NgR proteins displayed only a moderate reduction of MAG-mediated inhibition of neurite growth. If treated with Vibrio cholerae neuraminidase (VCN), inhibition by MAG is further attenuated but still not annulled. Thus, disrupting all known protein and ganglioside receptors for MAG in sensory neurons does not fully abolish its inhibitory activity pointing to the existence of as yet unidentified receptors for MAG. Moreover, by employing a variety of protein mutants, we identified the Ig-like domains 4 or 5 of MAG as necessary and sufficient for growth arrest, whereas abolishing MAG's ability to bind to sialic acid did not interfere with its inhibitory activity. These findings provide new insights into the inhibitory function of MAG and suggest similarities but also major differences in MAG inhibition between sensory and central nervous system (CNS) neurons.
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