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New roles for glial cell line-derived neurotrophic factor and neurturin -: Involvement in hair cycle control

AMERICAN JOURNAL OF PATHOLOGY 2000年第3期156卷 1041-1053页

作者： Botchkareva, NV Botchkarev, VA Welker, P Airaksinen, M Roth, W Suvanto, P Müller-Röver, S Hadshiew, IM Peters, C Paus, R Univ Hamburg Hosp Eppendorf Dept Dermatol D-20246 Hamburg Germany Humboldt Univ Charite Dept Dermatol Berlin Germany Univ Helsinki Inst Biotechnol Helsinki Finland Univ Freiburg Inst Mol Med Freiburg Germany

Glial cell line-derived neurotrophic factor (GDNF), neurturin (NTN), and their receptors, GDNF family receptor alpha-1. (GFR alpha-1) and GDNF family receptor alpha-2 (GFR alpha-2), are critically important for kidney and nervous system development. However, their role in skin biology, specifically in hair growth control, is as yet unknown. We have studied expression and function of GDNF, neurturin, GFR alpha-1, and GFR alpha-2 in murine skin during the cyclic transformation of the hair follicle (HF) from its resting state (telogen) to active growth (anagen) and then through regression (catagen) back to telogen. GDNF protein and GFR alpha-1 messenger RNA are prominently expressed in telogen skin, which lacks NTN and GFR alpha-2 transcripts. Early anagen development is accompanied by a significant decline in the skin content of GDNF protein and GFR alpha-1 transcripts. During the anagen-catagen transition, GDNF, GFR alpha-1, NTN, and GFR alpha-2 transcripts reach maximal levels. Compared with wild-type controls, GFR alpha-1 (+/-) and GFR alpha-2 (-/-) knockout mice show a significantly accelerated catagen development. Furthermore, GDNF or NTN administration significantly retards HF regression in organ-cultured mouse skin. This suggests important, previously unrecognized roles for GDNF/GFR alpha-1 and NTN/GFR alpha-2 signaling in skin biology, specifically in the control of apoptosis-driven HF involution, and raises the possibility that GFR alpha-1/GFR alpha-2 agonists/antagonists might become exploitable for the treatment of hair growth disorders that are related to abnormalities in catagen development.

关键词：动物新生细胞培养的 DNA/分析 DNA引物/化学果蝇蛋白质类酶联免疫吸附测定胶质细胞源性神经营养因子胶质细胞源性神经营养因子受体毛囊/药物作用毛囊/生长和发育毛发去除杂合子纯合子原位杂交小鼠近交C57BL 小鼠基因敲除神经生长因子类/代谢神经生长因子类/药理学神经组织蛋白质类/代谢神经组织蛋白质类/药理学 Neurturin神经营养因子原癌基因蛋白质类/遗传学原癌基因蛋白质类/代谢原癌基因蛋白质c-ret RNA 信使/代谢受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/代谢逆转录聚合酶链反应皮肤/代谢动物女(雌)性小鼠

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The neuregulin receptor ErbB-4 interacts with PDZ-containing proteins at neuronal synapses

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第7期97卷 3596-3601页

作者： Garcia, RAG Vasudevan, K Buonanno, A NIH Mol Neurobiol Unit Bethesda MD 20892 USA

Neuregulins regulate the expression of ligand- and voltage-gated channels in neurons and skeletal muscle by the activation of their cognate tyrosine kinase receptors, ErbB 1-4. The subcellular distribution and mechanisms that regulate the localization of ErbB receptors are unknown. We have found that ErbB receptors are present in brain subcellular fractions enriched for postsynaptic densities (PSD). The ErbB-4 receptor is unique among the ErbB proteins because its C-terminal tail (T-V-V) conforms to a sequence that binds to a protein motif known as the PDZ domain, Using the yeast two-hybrid system, we found that the C-terminal region of ErbB-4 interacts with the three related membrane-associated guanylate kinases (MAGUKs) PSD-95/SAP90. PSD-93/chapsyn-110, and SAP 102, which harbor three PDZ domains, as well as with beta(2)-syntrophin, which has a single PDZ domain, As with N-methyl-D-aspartate (NMDA) receptors, ErbB-4 interacts with the first two PDZ domains of PSD-95, Using coimmunoprecipitation assays, we confirmed the direct interactions between ErbB-4 and PSD-95 in transfected heterologous cells, as well as in vivo, where both proteins are coimmunoprecipitated from brain lysates. Moreover, evidence for colocalization of these proteins was also observed by immunofluorescence in cultured hippocampal neurons. ErbB-4 colocalizes with PSD-95 and NMDA receptors at a subset of excitatory synapses apposed to synaptophysin-positive presynaptic terminals, The capacity of ErbB receptors to interact with PDZ-domain proteins at cell junctions is conserved from invertebrates to mammals. As discussed, the interactions found between receptor tyrosine kinases and MAGUKs at neuronal synapses may have important implications for activity-dependent plasticity.

关键词：碱基序列细胞培养的 DNA引物鸟苷酸激酶海马/细胞学海马/代谢免疫组织化学神经组织蛋白质类/代谢神经元/代谢蛋白质结合大鼠 Sprague-Dawley 受体表皮生长因子/代谢突触/代谢肿瘤抑制蛋白质类动物大鼠

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Dorfin localizes to the ubiquitylated inclusions in Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and amyotrophic lateral sclerosis

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 609-619页

作者： Hishikawa, N Niwa, J Doyu, M Ito, T Ishigaki, S Hashizume, Y Sobue, G Nagoya Univ Grad Sch Med Dept Neurol Nagoya Aichi 4668550 Japan Aichi Med Univ Dept Neuropathol Inst Med Sci Aging Aichi Japan

In many neurodegenerative diseases, the cytopathological hallmark is the presence of ubiquitylated inclusions consisting of insoluble protein aggregates. Lewy bodies in Parkinson's disease and dementia with Lewy bodies disease, glial cell inclusions in multiple system atrophy, and hyaline inclusions in amyotrophic lateral sclerosis (ALS) are representative of these inclusions. The elucidation of the components of these inclusions and the mechanisms underlying inclusion formation is important in uncovering the pathogenesis of these disorders. We hypothesized that Dorfin, a perinuclearly located E3 ubiquitin ligase, participates in the formation of ubiquitylated inclusions in a wide range of neurodegenerative diseases. Here, we report that affinity-purified anti-Dorfin antibody labeled ubiquitylated inclusions of Parkinson's disease, dementia with Lewy bodies disease, multiple system atrophy, and sporadic and familial ALS. A double-immunofluorescence study revealed that Dorfin shows a distribution pattern parallel to that of ubiquitin. Furthermore, by a filter trap assay, we detected that Dorfin is present in the ubiquitylated high-molecular weight structures derived from these diseases. These results suggest that Dorfin plays a crucial role in the formation of ubiquitylated inclusions of alpha-synucleinopathy and ALS. However, because we failed to show the direct binding of a-synuclein with Dorfin, future investigations into the binding partner(s) of Dorfin will be needed to deepen our understanding of the pathophysiology of alpha-synucleinopathy and ALS.

关键词：肌萎缩侧索硬化/代谢肌萎缩侧索硬化/病理学抗体/代谢细胞系 DNA结合蛋白质类/代谢包涵体/代谢 Lewy体病/代谢 Lewy体病/病理学分子量多系统萎缩/代谢多系统萎缩/病理学神经组织蛋白质类/代谢神经胶质/代谢神经胶质/超微结构神经元/代谢神经元/超微结构帕金森病/代谢帕金森病/病理学蛋白质结合超氧化物歧化酶/代谢突触核蛋白类泛素/代谢泛素蛋白连接酶类 α突触核蛋白老年人女(雌)性人类男(雄)性中年人

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Developmental profiles of growth-associated protein (Gap43), Ngfb, Bndf and Ntf4 mRNA levels in the rat forebrain after exposure to 60 Hz magnetic fields

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RADIATION RESEARCH 2000年第5期153卷 642-647页

作者： Harry, GJ Bartenbach, M Haines, W Bruccoleri, A NIEHS Neurotoxicol Grp Res Triangle Pk NC 27709 USA

Fischer 344 rats were exposed to 60 Hz magnetic fields (EMFs) during gestation and lactation. Rats received continuous exposure to 2-, 200- or 1000-mu T magnetic fields for 18.5 h per day, 7 days a week, or sham exposure (sham controls). During postnatal development, on postnatal days 1, 3, 6, 9, 15 and 20, forebrain tissue from male pups was examined for alterations in mRNA level for developmentally regulated central nervous system-specific proteins. Alterations in these factors during critical periods of development could result in alterations in the final neural network. Gap43 (growth-associated protein 43) mRNA was measured by Northern hybridization as a developmental indicator of axonal growth during the development of the neuron. Between postnatal days 1 and 9, detectable levels of Gap43 mRNA displayed a similar pattern across all sham control and exposure groups. In addition to Gap43, mRNA levels for the nervous system-specific growth factors ciliary neurotrophic factor (Cntf), brain-derived neurotrophic factor (Bdnf), beta nerve growth factor (Ngfb), neurotrophin-3 (Ntf3), and neurotrophin-4 (Ntf4) were examined by RNase protection assay. While there is public concern for developmental neurotoxicity associated with exposure to EMFs, these data, generated from animals exposed to 2-, 200 or 1000-mu T magnetic fields during both gestational and lactational periods of development, suggest that under these conditions no significant alterations in these critical factors for brain development occur. (C) 2000 by Radiation Research Society.

关键词：动物新生动物吮乳期脑源性神经营养因子/遗传学脑源性神经营养因子/代谢剂量效应关系辐射电磁场/副作用环境暴露/副作用 GAP-43蛋白/遗传学 GAP-43蛋白/代谢胶质细胞源性神经营养因子母亲暴露/副作用神经生长因子/遗传学神经生长因子/代谢神经生长因子类/遗传学神经生长因子类/代谢神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经营养因子3/遗传学神经营养因子3/代谢前脑/生长和发育前脑/代谢前脑/辐射效应 RNA 信使/分析大鼠近交F344 大鼠 Sprague-Dawley 核糖核酸酶类/代谢动物女(雌)性男(雄)性大鼠

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Interaction of NE-dlg/SAP102, a neuronal and endocrine tissue-specific membrane-associated guanylate kinase protein, with calmodulin and PSD-95/SAP90 - A possible regulatory role in molecular clustering at synaptic sites

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第9期274卷 5782-5790页

作者： Masuko, N Makino, K Kuwahara, H Fukunaga, K Sudo, T Araki, N Yamamoto, H Yamada, Y Miyamoto, E Saya, H Kumamoto Univ Sch Med Dept Tumor Genet & Biol Kumamoto 8600811 Japan Kumamoto Univ Sch Med Dept Pharmacol Kumamoto 8600811 Japan Taisho Pharmaceut Co Ltd Hanno Res Ctr Canc Res Lab Hanno Saitama 3578527 Japan

NE-dlg/SAP102, a neuronal and endocrine tissue-specific membrane-associated guanylate kinase family protein, is known to bind to C-terminal ends of N-methyl-D-aspartate receptor 2B (NR2B) through its PDZ (PSD-95/Dlg/ZO-1) domains. NE-dlg/SAP102 and NR2B colocalize at synaptic sites in cultured rat hippocampal neurons, and their expressions increase in parallel with the onset of synaptogenesis, me have identified that NE-dlg/SAP102 interacts with calmodulin in a Ca2+-dependent manner. The binding site for calmodulin has been determined to he at the putative basic cr-helix region located around the src homology 3 (SH3) domain of NE-dlg/SAP102. Using a surface plasmon resonance measurement system, we detected specific binding of recombinant NE-dlg/SAP102 to the immobilized calmodulin with a K-d value of 44 nM. However, the binding of Ca2+/calmodulin to NE-dlg/SAP102 did not modulate the interaction between PDZ domains of NE-dlg/SAP102 and the C-terminal end of rat NR2B. We have also identified that the region near the calmodulin binding site of NE-dlg/SAP102 interacts with the GUK-like domain of PSD-95/SAP90 by two-hybrid screening. Pull down assay revealed that NE-dlg/SAP102 can interact with PSD-95/SAP90 in the presence of both Ca2+ and calmodulin. These findings suggest that the Ca2+/calmodulin modulates interaction of neuronal membrane-associated guanylate kinase proteins and regulates clustering of neurotransmitter receptors at central synapses.

关键词：氨基酸序列碱基序列钙调蛋白/代谢细胞培养的 DNA引物海马/细胞学海马/代谢分子序列数据神经组织蛋白质类/代谢神经元/代谢神经肽类/代谢蛋白质结合序列同源性氨基酸信号传导动物大鼠

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Hsp70 and Hsp40 chaperones can inhibit self-assembly of polyglutamine proteins into amyloid-like fibrils

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第14期97卷 7841-7846页

作者： Muchowski, PJ Schaffar, G Sittler, A Wanker, EE Hayer-Hartl, MK Hartl, FU Max Planck Inst Biochem Dept Cellular Biochem D-82152 Martinsried Germany Max Planck Inst Mol Genet D-14195 Berlin Dahlem Germany

The deposition of protein aggregates in neurons is a hallmark of neurodegenerative diseases caused by polyglutamine (polyQ) proteins. We analyzed the effects of the heat shock protein (Hsp) 70 chaperone system on the aggregation of fragments of huntingtin (htt) with expanded polyQ tracts. In vitro, Hsp70 and its cochaperone Hsp40 suppressed the assembly of htt into detergent-insoluble amyloid-like fibrils in an ATP-dependent manner and caused the formation of amorphous, detergent-soluble aggregates. The chaperones were most active in preventing fibrillization when added during the lag phase of the polymerization reaction. Similarly, coexpression of Hsp70 or Hsp40 with htt in yeast inhibited the formation of large, detergent-insoluble polyQ aggregates, resulting in the accumulation of detergent-soluble inclusions. Thus, the recently established potency of Hsp70 and Hsp40 to repress polyQ-induced neurodegeneration may be based on the ability of these chaperones to shield toxic forms of polyQ proteins and to direct them into nontoxic aggregates.

关键词：氨基酸序列淀粉样蛋白/代谢淀粉样蛋白/超微结构监控蛋白60/代谢监控蛋白类/代谢外显子 HSP40热休克蛋白质类热休克蛋白质类/代谢分子序列数据神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经组织蛋白质类/超微结构核蛋白质类/遗传学核蛋白质类/代谢核蛋白质类/超微结构肽碎片/遗传学肽碎片/代谢肽碎片/超微结构肽类/遗传学肽类/代谢蛋白质结合重组融合蛋白质类/代谢酵母菌酿酒/遗传学酵母菌酿酒/代谢三核苷酸重复扩增人类

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A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration

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NEURON 1999年第1期23卷 181-192页

作者： Hodgson, JG Agopyan, N Gutekunst, CA Leavitt, BR LePiane, F Singaraja, R Smith, DJ Bissada, N McCutcheon, K Nasir, J Jamot, L Li, XJ Stevens, ME Rosemond, E Roder, JC Phillips, AG Rubin, EM Hersch, SM Hayden, MR Univ British Columbia Ctr Mol Med & Therapeut Vancouver BC V5Z 4H4 Canada Univ British Columbia Dept Psychol Vancouver BC V6T 1Z4 Canada Univ Toronto Fac Pharm Toronto ON L4V 1V7 Canada Univ Toronto Dept Mol Immunol & Neurobiol Toronto ON M5G 1X5 Canada Emory Univ Sch Med Atlanta GA 30322 USA Univ Calif Berkeley Lawrence Berkeley Lab Ctr Human Genome Berkeley CA 94720 USA

We have produced yeast artificial chromosome (YAC) transgenic mice expressing normal (YAC18) and mutant (YAC46 and YAC72) huntingtin (htt) in a developmental and tissue-specific manner identical to that observed in Huntington's disease (HD). YAC46 and YAC72 mice show early electrophysiological abnormalities, indicating cytoplasmic dysfunction prior to observed nuclear inclusions or neurodegeneration. By 12 months of age, YAC72 mice have a selective degeneration of medium spiny neurons in the lateral striatum associated with the translocation of N-terminal htt fragments to the nucleus. Neurodegeneration can be present in the absence of macro- or microaggregates, clearly showing that aggregates are not essential to initiation of neuronal death. These mice demonstrate that initial neuronal cytoplasmic toxicity is followed by cleavage of htt, nuclear translocation of htt N-terminal fragments, and selective neurodegeneration.

关键词：适应生理学/生理学行为动物/生理学脑/病理学染色体人工酵母/遗传学纹状体/病理学细胞质/病理学疾病模型动物电生理学胚胎哺乳动物/生理学杭廷顿病/遗传学杭廷顿病/代谢杭廷顿病/病理学杭廷顿病/病理生理学小鼠近交系小鼠转基因/遗传学运动活动/生理学突变/生理学神经变性/病理学神经组织蛋白质类/遗传学神经组织蛋白质类/代谢核蛋白质类/遗传学核蛋白质类/代谢动物小鼠

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Rapid aggregate formation of the huntingtin N-terminal fragment carrying an expanded polyglutamine tract

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第2期256卷 361-366页

作者： Hazeki, N Nakamura, K Goto, J Kanazawa, I Univ Tokyo Grad Sch Med Dept Neurol Div NeurosciBunkyo Ku Tokyo 1138655 Japan Japan Sci & Technol Corp CREST Tokyo Japan

Huntington's disease (HD) is caused by an expansion of the CAG repeat in the HD gene. The repeat is translated to the polyglutamine tract as huntingtin, the product of HD gene. Several studies showed that the expansion of polyglutamine tract leads to formation of cytoplasminc and/or intranuclear aggregates in vivo or in vitro. To understand the molecular mechanism of the aggregate formation, we studied the transient expression of HD exon 1-GFP fusion proteins in COS-7 cells. The fusion protein carrying 77 glutamine repeats aggregated in a time-dependent manner, while the fusion protein carrying 25 glutamine tract remained to be distributed diffusely in the cytoplasm even 72 hours after transfection. Initially, fluorescent signals were diffusely distributed in the COS-7 cells that were transfected with the construct containing the 77 CAG repeats. Approximately 40 hours later after the transfection, large aggregates grew very rapidly in those cells and the diffuse cytoplasmic fluorescence faded out. This process was completed within 40 minutes from the appearance of small aggregates in the perinuclear regions, The addition of cycloheximide reduced the frequencies of aggregate formation. A possibility was discussed that the aggregate formation was via nucleation. The focal concentration of mutated proteins in neurons may trigger the aggregate formation. (C) 1999 Academic Press.

关键词：印迹法蛋白质 COS细胞细胞核/代谢放线菌酮/药理学细胞松弛素D/药理学细胞质/代谢外显子/遗传学杭廷顿病/遗传学杭廷顿病/代谢分子量神经组织蛋白质类/生物合成神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/代谢诺考达唑/药理学核蛋白质类/生物合成核蛋白质类/化学核蛋白质类/遗传学核蛋白质类/代谢紫杉酚/药理学肽碎片/生物合成肽碎片/化学肽碎片/遗传学肽碎片/代谢肽类/化学肽类/遗传学肽类/代谢蛋白质结合/药物作用重组融合蛋白质类/生物合成重组融合蛋白质类/化学重组融合蛋白质类/代谢时间因素转染衣霉素/药理学动物人类

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Uteroplacental insufficiency alters cerebral mitochondrial gene expression and DNA in fetal and juvenile rats

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PEDIATRIC RESEARCH 2000年第6期47卷 792-797页

作者： Lane, RH Tsirka, AE Gruetzmacher, EM Univ Calif Los Angeles Mattel Childrens Hosp Sch Med Dept Pediat Los Angeles CA 90095 USA Univ Pittsburgh Magee Womens Res Inst Sch Med Dept Pediat Pittsburgh PA 15213 USA

Uteroplacental insufficiency increases the risk of perinatal and long-term neurologic morbidity by depriving the fetus of oxidative substrate and causing intrauterine growth retardation. Skeletal muscle and liver from growth retarded fetal and juvenile rats respond to this deprivation by altering mitochondrial gene expression and function. The objective of this study was to determine whether cerebral mitochondrial mRNA is similarly altered in fetal and juvenile growth retarded rats and to correlate these alterations with mitochondrial DNA and marker protein levels. To fulfill this objective, mRNA levels of four important mitochondrial proteins were quantified using RT-PCR in growth retarded and sham-operated control fetal and juvenile rat brains;these proteins were NADH-ubiquinone oxireductase subunit 4, subunit C of the F1F0-ATPase, and the adenine nucleotide transporters 1 and 2. Mitochondrial DNA/nuclear DNA ratios and mitochondrial 60 kD marker protein levels were also quantified in growth retarded and sham-operated control fetal and juvenile rat brains using PCR and Western Blotting, respectively. Cerebral mRNA levels of all four proteins were increased in the IUGR fetuses and decreased in the IUGR juvenile animals. Cerebral mitochondrial/nuclear DNA ratios and mitochondrial marker protein levels were not significantly altered in the IUGR fetuses;however, both were significantly diminished in IUGR juvenile pups. These studies suggest that the metabolic stresses associated with uteroplacental insufficiency in the rat cause altered fetal and postnatal cerebral mitochondrial mRNA and DNA levels.

关键词：碱基序列脑/代谢 DNA引物 DNA 线粒体/代谢胎儿生长迟缓基因表达谱线粒体/代谢神经组织蛋白质类/代谢胎盘血液循环/遗传学 RNA 信使/遗传学大鼠 Sprague-Dawley 逆转录聚合酶链反应动物女(雌)性妊娠大鼠

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Regulation of neuregulin signaling by PSD-95 interacting with ErbB4 at CNS synapses

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NEURON 2000年第2期26卷 443-455页

作者： Huang, YZ Won, S Ali, DW Wang, Q Tanowitz, M Du, QS Pelkey, KA Yang, DJ Xiong, WC Salter, MW Mei, L Univ Alabama Birmingham Dept Neurobiol Pathol & Phys Med & Rehabil Birmingham AL 35294 USA Univ Virginia Dept Pharmacol Charlottesville VA 22908 USA Chinese Acad Sci Inst Neurosci Mol Neurobiol Lab Shanghai 200031 Peoples R China Shanghai Res Ctr Life Sci Shanghai 200031 Peoples R China Univ Toronto Hosp Sick Children Dept Physiol Program Brain & Behav Toronto ON M5G 1X8 Canada Univ Toronto Hosp Sick Children Dept Physiol Cell Biol Program Toronto ON M5G 1X8 Canada Georgetown Univ Vincent T Lombardi Canc Res Ctr Washington DC 20007 USA Univ Alabama Birmingham Dept Pathol Birmingham AL 35294 USA

Neuregulins (NRGs) and their receptors, the ErbB protein tyrosine kinases, are essential for neuronal development, but their functions in the adult CNS are unknown. We report that ErbB4 is enriched in the postsynaptic density (PSD) and associates with PSD-95. Heterologous expression of PSD-95 enhanced NRG activation of ErbB4 and MAP kinase. Conversely, inhibiting expression of PSD-95 in neurons attenuated NRG-mediated activation of MAP kinase. PSD-95 formed a ternary complex with two molecules of ErbB4, suggesting that PSD-95 facilitates ErbB4 dimerization. Finally, NRG suppressed induction of long-term potentiation in the hippocampal CA1 region without affecting basal synaptic transmission. Thus, NRG signaling may be synaptic and regulated by PSD-95. A role of NRG signaling in the adult CNS may be modulation of synaptic plasticity.

关键词：脑/细胞学脑/生理学细胞培养的电刺激海马/细胞学海马/代谢海马/生理学细胞内信号肽和蛋白质类长时程增强/药物作用膜蛋白质类神经组织蛋白质类/代谢神经组织蛋白质类/生理学神经调节蛋白类/药理学神经调节蛋白类/生理学神经元/代谢信号传导/生理学突触/生理学组织分布酵母菌动物大鼠

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