β-Amyloid42 Induces Desensitization of CXC Chemokine Receptor-4 via Formyl Peptide Receptor in Neural Stem/Progenitor Cells
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- 資料種別
- 記事
- 著者・編者
- Can ZhangZe-Jian WangKeng-Hoe Lok 他
- タイトル（掲載誌）
- Biological and pharmaceutical bulletin
- 巻号年月日等（掲載誌）
- 35(2):2012.2
- 掲載巻
- 35
- 掲載号
- 2
- 掲載ページ
- 131-138
- 掲載年月日（W3CDTF）
- 2012-02
- ISSN（掲載誌）
- 0918-6158
- ISSN-L（掲載誌）
- 0918-6158
- 出版事項（掲載誌）
- Tokyo : Pharmaceutical Society of Japan
- 出版地（国名コード）
- JP
- 本文の言語コード
- eng
- 件名標目
- NDLC
- 対象利用者
- 一般
- 所蔵機関
- 国立国会図書館
- 請求記号
- Z53-V41
- 連携機関・データベース
- 国立国会図書館 : 国立国会図書館雑誌記事索引
- 書誌ID（NDLBibID）
- 023408339
- 整理区分コード
- 632
- 要約等
- The deposition of β-amyloid (Aβ) plaques and progressive loss of neurons are two main characteristics of Alzheimer’s disease (AD). Supplement of neural stem/progenitor cells (NSPCs) is a promising strategy for repair of the neurodegenerative diseases. However, hostile microenvironment of neurodegenerative brain is harmful for the neuroregeneration. Aβ<sub>42</sub> promoted the proliferation of NSPCs. Moreover, Aβ<sub>42</sub> (10—1000 n<small>M</small>) promoted the migration of NSPCs in a dose-dependent manner. The attraction of NSPCs toward Aβ<sub>42</sub> was significantly offset by 10 μ<small>M</small> cyclosporin H, a potent and selective formyl peptide receptor antagonist. After incubation with Aβ<sub>42</sub> for 9 d, the migration ability of NSPCs was significantly decreased (<i>p</i><0.05). The expression of formyl peptide receptor (FPR) and CXC chemokine receptor-4 (CXCR4) were significantly decreased in NSPCs. The expression of G protein-coupled receptor kinase 2 (GRK2) was up-regulated on the membrane of NSPCs correspondingly. Our results suggested that Aβ<sub>42</sub> decreases the migratory capacity of NSPCs by FPR heterologous desensitization after long time incubation, and GRK2 in NSPCs may be responsible for the damaged migratory capacity.
- DOI
- 10.1248/bpb.35.131
- オンライン閲覧公開範囲
- インターネット公開
- 連携機関・データベース
- 科学技術振興機構 : J-STAGE
- 要約等
- The deposition of β-amyloid (Aβ) plaques and progressive loss of neurons are two main characteristics of Alzheimer’s disease (AD). Supplement of neural stem/progenitor cells (NSPCs) is a promising strategy for repair of the neurodegenerative diseases. However, hostile microenvironment of neurodegenerative brain is harmful for the neuroregeneration. Aβ<sub>42</sub> promoted the proliferation of NSPCs. Moreover, Aβ<sub>42</sub> (10—1000 n<small>M</small>) promoted the migration of NSPCs in a dose-dependent manner. The attraction of NSPCs toward Aβ<sub>42</sub> was significantly offset by 10 μ<small>M</small> cyclosporin H, a potent and selective formyl peptide receptor antagonist. After incubation with Aβ<sub>42</sub> for 9 d, the migration ability of NSPCs was significantly decreased (<i>p</i><0.05). The expression of formyl peptide receptor (FPR) and CXC chemokine receptor-4 (CXCR4) were significantly decreased in NSPCs. The expression of G protein-coupled receptor kinase 2 (GRK2) was up-regulated on the membrane of NSPCs correspondingly. Our results suggested that Aβ<sub>42</sub> decreases the migratory capacity of NSPCs by FPR heterologous desensitization after long time incubation, and GRK2 in NSPCs may be responsible for the damaged migratory capacity.
- DOI
- 10.1248/bpb.35.131
- 関連情報（URI）
- 参照
- Extension of Long Leading Processes and Neuronal Migration in the Mammalian Brain Directed by the Chemoattractant Netrin-1Regeneration of Hippocampal Pyramidal Neurons after Ischemic Brain Injury by Recruitment of Endogenous Neural ProgenitorsOverexpression of GRK2 in alzheimer disease and in a chronic hypoperfusion rat model is an early marker of brain mitochondrial lesionsThe netrins define a family of axon outgrowth-promoting proteins homologous to C. elegans UNC-6Cyclosporin H is a potent and selective formyl peptide receptor antagonist. Comparison with N-t-butoxycarbonyl-L-phenylalanyl-L-leucyl-L-phenylalanyl-L- leucyl-L-phenylalanine and cyclosporins A, B, C, D, and ERestricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zoneProtein signaling pathways in differentiation of neural stem cellsNeuronally expressed stem cell factor induces neural stem cell migration to areas of brain injuryPlatelet-derived growth factor induces chemotaxis of neuroepithelial stem cellsNetrins are diffusible chemotropic factors for commissural axons in the embryonic spinal cordAβ1–42 stimulates adult SVZ neurogenesis through the p75 neurotrophin receptorStem Cell Therapy for Alzheimers DiseaseDESENSITIZATION OF G PROTEIN–COUPLED RECEPTORS AND NEURONAL FUNCTIONSShort-Range and Long-Range Guidance by Slit and Its Robo ReceptorsAdhesion receptor expression by hematopoietic cell lines and murine progenitorsHYPOXIA‐INDUCED ASTROCYTES PROMOTE THE MIGRATION OF NEURAL PROGENITOR CELLS VIA VASCULAR ENDOTHELIAL FACTOR, STEM CELL FACTOR, STROMAL‐DERIVED FACTOR‐1α AND MONOCYTE CHEMOATTRACTANT PROTEIN‐1 UPREGULATION <i>IN VITRO</i>Broad immunocytochemical localization of the formylpeptide receptor in human organs, tissues, and cellsDisruption of neurogenesis by amyloid β‐peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's diseaseDirected migration of neural stem cells to sites of CNS injury by the stromal cell-derived factor 1α/CXC chemokine receptor 4 pathwayThe cell biology of neuronal navigationThe complex G protein‐coupled receptor kinase 2 (GRK2) interactome unveils new physiopathological targetsMicroglial activation depends on beta‐amyloid conformation: role of the formylpeptide receptor 2Stem cell bioengineering for regenerative medicineslit: an extracellular protein necessary for development of midline glia and commissural axon pathways contains both EGF and LRR domains.Embryonic stem cell-derived neural precursor cells improve memory dysfunction in Aβ(1–40) injured ratsNeurogenesis in mouse models of Alzheimer's diseaseG protein-coupled receptors stimulation and the control of cell migrationDirectional guidance of neuronal migration in the olfactory system by the protein SlitReceptors for chemotactic formyl peptides as pharmacological targetsThe Timing of Differentiation of Adult Hippocampal Neurons Is Crucial for Spatial MemoryMiR-125b promotes proliferation and migration of type II endometrial carcinoma cells through targeting TP53INP1 tumor suppressor in vitro and in vivoTargeted migration and differentiation of engrafted neural precursor cells in amyloid β-treated hippocampus in ratsLymphocyte G-protein-coupled receptor kinase-2 is upregulated in patients with Alzheimer's diseaseAmyloid β<sub>42</sub>Activates a G-Protein-Coupled Chemoattractant Receptor, FPR-Like-1Effects of the monomeric, oligomeric, and fibrillar Aβ<sub>42</sub> peptides on the proliferation and differentiation of adult neural stem cells from subventricular zoneEGF Transregulates Opioid Receptors through EGFR-mediated GRK2 Phosphorylation and ActivationWnt signaling pathway overcomes the disruption of neuronal differentiation of neural progenitor cells induced by oligomeric amyloid β-peptide
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- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
- Japan Link Center雑誌記事索引データベースCrossrefCiNii Articles
- 書誌ID（NDLBibID）
- 023408339
- NII論文ID
- 130001872285