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Image Search Results
Journal: Advanced Pharmaceutical Bulletin
Article Title: Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells
doi: 10.15171/apb.2020.008
Figure Lengend Snippet: The sequence of primers for alpha7 nicotinic acetylcholine receptor (α7nAChR), caspase-3, cyclin B1, and GAPDH genes
Article Snippet: The primers sequences for
Techniques: Sequencing
Journal: British Journal of Pharmacology
Article Title: Hippocampal α7 nicotinic ACh receptors contribute to modulation of depression‐like behaviour in C57BL/6J mice
doi: 10.1111/bph.13769
Figure Lengend Snippet: Experimental design for pharmacological and molecular genetic manipulations
Article Snippet: Prenatal stress, which can induce depression‐like phenotypes, decreases
Techniques: Saline, Knockdown, shRNA, Suspension
Journal: British Journal of Pharmacology
Article Title: Hippocampal α7 nicotinic ACh receptors contribute to modulation of depression‐like behaviour in C57BL/6J mice
doi: 10.1111/bph.13769
Figure Lengend Snippet: Effect of α7 nAChR knockdown on behaviour in tests of depression‐like phenotypes. Time spent immobile in (A) the tail suspension and (B) forced swim tests following α7 nAChR knockdown in the hippocampus of C57BL/6J male mice. In the forced swim test, data are split into 5‐ and 10‐min time bins and represent the same assay; 10 animals were used per treatment group in the final analyses. Data are expressed as means ± SEM, and dots represent individual data points. Inset represents an example of viral infection (GFP‐positive cells in the dorsal hippocampus/DG). *P < 0.05, significantly different as indicated; ANOVA and partial least squares differences post hoc tests, for each time point.
Article Snippet: Prenatal stress, which can induce depression‐like phenotypes, decreases
Techniques: Knockdown, Suspension, Infection
Journal: IBRO Neuroscience Reports
Article Title: Electroacupuncture alleviates paradoxical sleep deprivation-induced postoperative hyperalgesia via a7nAChR mediated BDNF/TrkB-KCC2 signaling pathway in the spinal cord
doi: 10.1016/j.ibneur.2024.10.002
Figure Lengend Snippet: The protein expression of α7nAChR (n=10 in each group). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.
Article Snippet: The filter membranes were blocked with 5 % nonfat milk for 1 h at room temperature and incubated with the primary
Techniques: Expressing
Journal: IBRO Neuroscience Reports
Article Title: Electroacupuncture alleviates paradoxical sleep deprivation-induced postoperative hyperalgesia via a7nAChR mediated BDNF/TrkB-KCC2 signaling pathway in the spinal cord
doi: 10.1016/j.ibneur.2024.10.002
Figure Lengend Snippet: Schematic diagram of the fluorescence of α7nAChR in the spinal cord (n=10 in each group). Scale bars are 50 μm.
Article Snippet: The filter membranes were blocked with 5 % nonfat milk for 1 h at room temperature and incubated with the primary
Techniques: Fluorescence
Journal: PLoS ONE
Article Title: Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier
doi: 10.1371/journal.pone.0162641
Figure Lengend Snippet: A-B: Immunehistochemical analysis of vimentin (A) and α7 nAChR (B) expression in mouse brain cortex. Images (A and B) photographed at 200X magnification C: Western blotting analysis of vimentin, α7 nAChR, phospho-IKKα/β and P65 expression levels in mouse vascular endothelial cells.
Article Snippet: All mouse monoclonal (MMAb)/ rabbit polyclonal (RPAb) antibodies and other reagents were commercially obtained from the following sources: (A) MMAbs against vimentin (V9) (sc-6260), NF-kB (p65) (sc-109) and a RPAb against β-actin (sc-130657) from Santa Cruz Biotechnology (Santa Cruz, CA); (B) RPAbs against phospho-IKK α/β (Ser176/180) (#2697), phospho-ERK1/2 (Thr202/Tyr204) (#4370), and a MMAb against IkBa (#4814) from Cell Signaling Technology (Danvers, MA); (C) a RPAb recognizing phoshothreonine286 of CaM kinase II from Promega and a MMAb recognizing CaM kinase II from BD Biosciences; (D) a
Techniques: Expressing, Western Blot
Journal: PLoS ONE
Article Title: Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier
doi: 10.1371/journal.pone.0162641
Figure Lengend Snippet: Elevation of intracellular calcium flux in HBMEC stimulated with E44 or ZD1 strains. HBMEC transfected with siRNAs of a scrambled sequence (CON), vimentin (Vim KD) and α7 nAChR (A7 KD) were loaded with Fura-2 AM as described in Methods and Materials. The monolayer was monitored for intracellular calcium flux for 10 minutes with 4 s intervals under an automated fluorescent microscope. Monolayer cells were stimulated with E44 or ZD (10 8 CFU) at the 120 s time point. The intensity of fluorescence at 340 nm and 380 nm was measured. The ratios of intensity of fluorescence at 340 nm and 380 nm were calculated for each time interval and depicted as continuous lines in (A–C). (G) The y axis represents the ratio, and x axis represents time (s). The 340 nm/380 nm ratio changes in each treatment were calculated and subjected to statistical analysis. WT HBMEC without any pre-treatment served as a control and are defined as one-fold (1.0). (*P<0.05; **P<0.01).
Article Snippet: All mouse monoclonal (MMAb)/ rabbit polyclonal (RPAb) antibodies and other reagents were commercially obtained from the following sources: (A) MMAbs against vimentin (V9) (sc-6260), NF-kB (p65) (sc-109) and a RPAb against β-actin (sc-130657) from Santa Cruz Biotechnology (Santa Cruz, CA); (B) RPAbs against phospho-IKK α/β (Ser176/180) (#2697), phospho-ERK1/2 (Thr202/Tyr204) (#4370), and a MMAb against IkBa (#4814) from Cell Signaling Technology (Danvers, MA); (C) a RPAb recognizing phoshothreonine286 of CaM kinase II from Promega and a MMAb recognizing CaM kinase II from BD Biosciences; (D) a
Techniques: Transfection, Sequencing, Microscopy, Fluorescence, Control
Journal: PLoS ONE
Article Title: Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier
doi: 10.1371/journal.pone.0162641
Figure Lengend Snippet: E . coli K1 infection triggers IbeA-dependent activation of the vimentin signaling pathway at the host cell membrane. IbeA binds to its receptor Vim and co-receptor PSF that interact with α7n nAChR through lipid rafts. These communications trigger phosphorylation of signaling proteins (e.g., Vim, TAK1), which in turn activates the nuclear factor-kappaB (NF-κB) pathways via activation of the IκB kinase (IKK) complex. NF-κB activation resulted to the nuclear translocation of NF-κB, which induces the production of cytokines, chemokines, and others proinflammatory molecules in response to bacterial stimuli.
Article Snippet: All mouse monoclonal (MMAb)/ rabbit polyclonal (RPAb) antibodies and other reagents were commercially obtained from the following sources: (A) MMAbs against vimentin (V9) (sc-6260), NF-kB (p65) (sc-109) and a RPAb against β-actin (sc-130657) from Santa Cruz Biotechnology (Santa Cruz, CA); (B) RPAbs against phospho-IKK α/β (Ser176/180) (#2697), phospho-ERK1/2 (Thr202/Tyr204) (#4370), and a MMAb against IkBa (#4814) from Cell Signaling Technology (Danvers, MA); (C) a RPAb recognizing phoshothreonine286 of CaM kinase II from Promega and a MMAb recognizing CaM kinase II from BD Biosciences; (D) a
Techniques: Infection, Activation Assay, Membrane, Phospho-proteomics, Translocation Assay
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Expression levels of α7 nAChR and Aβ in the brains of patients with AD and normal brains. (A) Images of the immunofluorescence double staining in the control and AD groups. (B) Aβ is expressed in the cytoplasm and extracellular matrix of cells. It was also found highly expressed in the brain slices of patients with AD, whereas the expression levels were minimal in healthy control brain sections following immunofluorescence double staining. (C) α7 nAChR was found expressed in the cytoplasm and reduced expression levels were observed in brain sections of patients with AD compared with healthy human brain sections, following immunofluorescence double staining. The cell nuclei are stained in blue using DAPI. Aβ-positive neurons are indicated in red and α3 nAChR-positive neurons are green. Scale bar, 20 µm. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control group. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease; IOD, integrated optical density.
Article Snippet: The
Techniques: Expressing, Immunofluorescence, Double Staining, Control, Staining, Standard Deviation
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Mean IOD of α7 nAChR is negatively correlated with the mean IOD of Aβ in the brain of patients with AD. Mean IOD of α7 nAChR and Aβ were found to be negatively correlated with each other in the (A) temporal cortex, (B) frontal cortex and (C) hippocampus following immunofluorescence double staining of brain slices of patients with AD. Data was obtained using correlation analysis (n=9). P<0.05 α7 nAChR vs. Aβ. IOD, integrated optical density; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; Aβ, β-amyloid; AD, Alzheimer's disease.
Article Snippet: The
Techniques: Immunofluorescence, Double Staining
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Expression levels of α7 nAChR mRNA and protein in SH-SY5Y cells in which α7 nAChR is overexpressed or silenced. (A) mRNA and (B) protein expression levels of α7 nAChR in SH-SY5Y cells overexpressing α7 nAChR. (C) mRNA and (D) protein expression levels of α7 nAChR in SH-SY5Y cells with silenced α7 nAChR expression. β-actin was used as an internal standard. Expression levels were determined using reverse transcription-quantitative PCR and western blotting. Data are presented as the mean ± standard deviation (n=9).**P<0.01 vs. control. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; shRNA, short hairpin RNA.
Article Snippet: The
Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, Control, shRNA
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Expression levels of SYP, PSD-95 and SNAP-25 in SH-SY5Y cells overexpressing α7 nAChR or with silenced α7 nAChR expression. Expression levels of mRNA and protein were determined using reverse transcription-quantitative PCR and western blotting, respectively. mRNA and protein expression levels of (A) SYP, (B) PSD-95 and (C) SNAP-25 after α7 nAChR overexpression. mRNA and protein expression levels of (D) SYP, (E) PSD-95 and (F) SNAP-25 after α7 nAChR silencing. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control. SYP, synaptophysin; PSD-95, postsynaptic density of 95 kDa; SNAP-25, synaptosomal-associated protein of 25 kDa; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; shRNA, short hairpin RNA.
Article Snippet: The
Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Over Expression, Standard Deviation, Control, shRNA
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Concentration of ACh and the activity of AChE in SH-SY5Y cells in which expression of α7 nAChR was overexpressed or silenced.
Article Snippet: The
Techniques: Concentration Assay, Activity Assay, Expressing, Control, shRNA, Plasmid Preparation
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Expression levels of SYP, PSD-95 and SNAP-25 in SH-SY5Y cells following the overexpression of α7 nAChR or silencing of α7 nAChR, and exposure to AβO. mRNA and protein expression levels of (A) SYP, (B) PSD-95 and (C) SNAP-25 after α7 nAChR overexpression. mRNA and protein expression levels of (D) SYP, (E) PSD-95 and (F) SNAP-25 after α7 nAChR silencing. The expression levels of mRNA and protein were determined using reverse transcription-quantitative PCR and western blotting, respectively. Data are presented as the mean ± standard deviation (n=9). *P<0.05 and **P<0.01 vs. control; ## P<0.01, # P<0.05 vs. empty plasmid. SYP, synaptophysin; PSD-95, postsynaptic density of 95 kDa; SNAP-25, synaptosomal-associated protein of 25 kDa; α7 nAChR, nicotinic acetylcholine receptor α7 subunit; AβO, Aβ1-42 oligomer; shRNA, short hairpin RNA.
Article Snippet: The
Techniques: Expressing, Over Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, Control, Plasmid Preparation, shRNA
Journal: Molecular Medicine Reports
Article Title: Expression levels of the α7 nicotinic acetylcholine receptor in the brains of patients with Alzheimer's disease and their effect on synaptic proteins in SH-SY5Y cells
doi: 10.3892/mmr.2020.11253
Figure Lengend Snippet: Apoptotic rate of SH-SY5Y cells, which are simultaneously exposed to α7 nAChR overexpression or gene silencing and AβO. (A) Apoptotic rate was determined using flow cytometry and (B) data are presented as the mean ± standard deviation (n=9). **P<0.01 vs. control; # P<0.05 vs. control + AβO. α7 nAChR, nicotinic acetylcholine receptor α7 subunit; AβO, Aβ1-42 oligomer; shRNA, short hairpin RNA.
Article Snippet: The
Techniques: Over Expression, Flow Cytometry, Standard Deviation, Control, shRNA
Journal: The Journal of Neuroscience
Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease
doi: 10.1523/JNEUROSCI.21-12-04125.2001
Figure Lengend Snippet: Nicotine activation of ERK2 in hippocampal slices is mediated by α7 nAChRs. a, Quantitative immunoblot demonstrates that 500 μm nicotine stimulated ERK2 MAPK activity, which is antagonized by 1 μm MLA in hippocampal slices from mice heterozygous for the L250T α7 nAChR transgene. Basal, 1.00 ± 0.22; nicotine (nic), 2.33 ± 0.13; MLA + nicotine, 1.34 ± 0.14. *Significant difference from basal level; p < 0.01, post hocTukey multiple comparison test. Representative immunoblot results are depicted below the response histogram. ERK1 (topband) activation paralleled that of ERK2; however, absolute levels of phospho-ERK1 were far below ERK2 and were not quantified. Slices from wild-type animals did not exhibit significant ERK2 MAPK activation with nicotine treatment, likely because of the rapid desensitization kinetics of wild-type α7 nAChRs precluding biochemical detection of ERK2 MAPK activation (Seguela et al., 1995). b, Quantitative immunoblot demonstrates that ERK2 MAPK activation by nicotine in cultured rat hippocampal slices is blocked by 1 μm MLA. Basal, 1.01 ± 0.08; nicotine, 1.66 ± 0.13; MLA + nicotine, 1.22 ± 0.09. *Denotes nicotine stimulation is significantly different from basal level;p < 0.001, post hoc Tukey multiple comparison test. Representative immunoblot results are depictedbelow the response histogram.
Article Snippet:
Techniques: Activation Assay, Western Blot, Activity Assay, Comparison, Cell Culture
Journal: The Journal of Neuroscience
Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease
doi: 10.1523/JNEUROSCI.21-12-04125.2001
Figure Lengend Snippet: α7 nAChR is upregulated in hippocampus and DG of Tg2576 mice. a, Quantitative immunoblot of area CA1 and DG from 4, 13, and ∼20 month Tg2576 hippocampus reveals upregulation of α7 nAChR protein as early as 4 months. *Significantly higher α7 nAChR level than age-matched control animals (p < 0.03) by Student's ttest. Dashed line represents normalized control animal level; note the change in scale for ∼20 month animals. Filled bar, CA1; shaded bar, DG. b, Representative immunoblot for α7 nAChR level in Tg2576 and age-matched control animals.
Article Snippet:
Techniques: Western Blot, Control
Journal: The Journal of Neuroscience
Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease
doi: 10.1523/JNEUROSCI.21-12-04125.2001
Figure Lengend Snippet: Downstream targets of α7 nAChR activation in Tg2576 hippocampus exhibit dysregulation. ERK2 and CREB proteins undergo hyperactivation, followed by downregulation, as compared with age-matched control animals. Differences between Tg2576 and age-matched control animals were detected by quantitative immunoblot of area CA1 and DG from 4, 13, and ∼20 month Tg2576 hippocampus. Samples were evaluated for total and phospho-ERK2 MAPK (a, c) and total and phospho-CREB (b, d) levels in CA1 and DG, respectively. *Significant difference from age-matched control animal level (p ≤ 0.05) by Student'st test. Dashed line represents normalized control animal level. Filled bar, Total; shaded bar, phospho.
Article Snippet:
Techniques: Activation Assay, Control, Western Blot
Journal: The Journal of Neuroscience
Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease
doi: 10.1523/JNEUROSCI.21-12-04125.2001
Figure Lengend Snippet: Data summary for the parameters measured in hippocampi of Tg2576 mice at different ages as compared with age-matched control animals
Article Snippet:
Techniques: Control
Journal: The Journal of Neuroscience
Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease
doi: 10.1523/JNEUROSCI.21-12-04125.2001
Figure Lengend Snippet: Animals with elevated α7 nAChR level fail to perform to criteria in the Morris water maze. Scatter plot of the third probe trial performance of individual ∼20-month-old Tg2576 and control animals versus α7 nAChR protein levels in CA1 and DG.Dashed line indicates performance criterion.Filled squares, Control; filled diamonds, Tg.
Article Snippet:
Techniques: Control
Journal: The Journal of Neuroscience
Article Title: β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors: In Vitro and In Vivo Mechanisms Related to Alzheimer's Disease
doi: 10.1523/JNEUROSCI.21-12-04125.2001
Figure Lengend Snippet: Chronic exposure to Aβ42 leads to increased α7 nAChR protein in hippocampal slice cultures. Cultured rat hippocampal slices were exposed to 100 pm Aβ42 for 144 hr, and α7 nAChR protein was quantified by immunoblot. The data that are expressed are normalized to the α7 nAChR protein level in cultures that were left untreated. Representative immunoblot results are shownbelow the histogram. *Significant difference from control level (p < 0.0001) by Student'st test. Basal, 1.00 ± 0.11; Aβ42-treated, 2.35 ± 0.13.
Article Snippet:
Techniques: Cell Culture, Western Blot, Control