α7-nachr Search Results


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  • 91
    Millar Inc α7 nachr
    α7 Nachr, supplied by Millar Inc, used in various techniques. Bioz Stars score: 91/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Tocris α7 nachr
    Stimulation of <t>α7</t> <t>nAChR</t> blocks TNF-induced NF-κB activation in BMDMs in vitro and postoperative systemic inflammation
    α7 Nachr, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore α7 nachr
    Nicotine acts through <t>α7</t> nAChRs. a The absence of α7 <t>nAChR</t> was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values
    α7 Nachr, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology α7 nachr inhibitor
    Nicotine acts through <t>α7</t> nAChRs. a The absence of α7 <t>nAChR</t> was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values
    α7 Nachr Inhibitor, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GenePharma Company rat α7 nachr
    Nicotine acts through <t>α7</t> nAChRs. a The absence of α7 <t>nAChR</t> was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values
    Rat α7 Nachr, supplied by GenePharma Company, used in various techniques. Bioz Stars score: 88/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    The Jackson Laboratory α7 nachr subunit
    Nicotinic receptors on mouse BAL cells . (A) RT-PCR, agarose gel electrophoresis. Mouse BAL cells consistently express mRNAs coding for α9, β2 and β4 subunits. Subunit α10 shows an interindividual expression pattern. The mRNA for <t>α7</t> subunit was not found in BAL preparations, although it was easily detectable in brain homogenate, serving as a positive control. M = DNA marker, H 2 O = water control (B) Ratiometric [Ca 2+ ] i recordings. Mouse BAL cells isolated from C57BL6N, α7 <t>nAChR</t> knockout (α7 -/- ) and littermate control animals (α7 +/+ ) were stimulated with ATP (10 -4 M) in the presence or absence (Hepes) of nicotine (10 -4 M). Peak increases shown as mean ± SEM; cells taken from 6-9 coverslips for each experimental setup, p-values calculated by Mann-Whitney test.
    α7 Nachr Subunit, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    The Jackson Laboratory α7 nachr gene
    Intracellular calcium, CaMKII and MAPK are required for <t>α7-nAChR-mediated</t> depression of GABA A receptor responses in CG neurons A , paired traces as in showing GABA-induced responses 1 min before and 2 s after applying nicotine for 3 s using
    α7 Nachr Gene, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 85/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology α7 nachr
    Involvements of <t>α7</t> <t>nAChR,</t> and PI3K, JNK and PKC pathways in the induction of EP4 by nicotine ( A ) Acetylcholine increased the expression of EP4 induced by nicotine in dose-dependent in A549 cells. ( B ) Acetylcholinesterase decreased the expression of EP4 induced by nicotine in dose-dependent in A549 cells. ( C ) a-bungarotoxin of a a7 nAChR blocker, not dihydro-β-erythroidine of a α4 nAChR inhibitor, decreased the expression of EP4 induced by nicotine in A549 cells. ( D ) α7 nAChR siRNA (100 nM) decreased the expression of EP4 induced by nicotine in A549 cells. ( E ) a-bungarotoxin, a a7 nAChR blocker, decreased the proliferation induced by nicotine in A549 cells and H1838 cells. ( F ) The specific inhibitors of PI3-K (wortmannin, 1 μM), JNK (SP600125, 20 μM) reduced expression of EP4 induced by nicotine in A549 cells. ( G ) The specific inhibitors of ERK (PD98095, 20 μM), not P38 MAPK (SB239063, 10 μM) had a minor effect on reduction of EP4 induced by nicotine in A549 cells. ( H ) The specific inhibitors of PKC (calphostin C, 0.5 μM), not PKA (H89, 10 μM) reduced expression of EP4 induced by nicotine in A549 cells. GAPDH served as internal control for normalization purposes.
    α7 Nachr, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 174 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam anti α7 nachr
    Effects of oral choline treatment on the gene and protein expression levels, respectively, of <t>α7</t> <t>nAChR</t> (A and B), HIF-1α (C and D), and VEGF (E and F) in the ischemic cerebral cortex. Mean±SEM. n =3. b P
    Anti α7 Nachr, supplied by Abcam, used in various techniques. Bioz Stars score: 89/100, based on 118 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore α7 nachr antagonist mla
    Effects of oral choline treatment on the gene and protein expression levels, respectively, of <t>α7</t> <t>nAChR</t> (A and B), HIF-1α (C and D), and VEGF (E and F) in the ischemic cerebral cortex. Mean±SEM. n =3. b P
    α7 Nachr Antagonist Mla, supplied by Millipore, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam human α7 nachr
    Effects of oral choline treatment on the gene and protein expression levels, respectively, of <t>α7</t> <t>nAChR</t> (A and B), HIF-1α (C and D), and VEGF (E and F) in the ischemic cerebral cortex. Mean±SEM. n =3. b P
    Human α7 Nachr, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher α7 nachr
    <t>α7</t> <t>nAchR</t> activation induced upregulation of canonical Nrf2 antioxidant genes. a Pretreatment with GTS21 (15 and 30 μm) for 1 h resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, and GCLC, in astrocytes treated with LPS for 24 h. α7 nAchR antagonist MLA (1 μm) significantly reduced this effect indicating the specificity of this response. * p
    α7 Nachr, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 52 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GenePharma Company human α7 nachr
    <t>α7</t> <t>nAchR</t> activation induced upregulation of canonical Nrf2 antioxidant genes. a Pretreatment with GTS21 (15 and 30 μm) for 1 h resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, and GCLC, in astrocytes treated with LPS for 24 h. α7 nAchR antagonist MLA (1 μm) significantly reduced this effect indicating the specificity of this response. * p
    Human α7 Nachr, supplied by GenePharma Company, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bionomics Ltd α7 nachr
    <t>α7</t> <t>nAchR</t> activation induced upregulation of canonical Nrf2 antioxidant genes. a Pretreatment with GTS21 (15 and 30 μm) for 1 h resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, and GCLC, in astrocytes treated with LPS for 24 h. α7 nAchR antagonist MLA (1 μm) significantly reduced this effect indicating the specificity of this response. * p
    α7 Nachr, supplied by Bionomics Ltd, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    OriGene α7 nachr
    <t>α7</t> <t>nAchR</t> negatively regulates inflammasome activation. (A) LPS-primed peritoneal mouse macrophages from either WT or α7 nAchR knockout (a7 KO) mice were stimulated with ATP in the presence or the absence of acetylcholine for 30 min. (B)
    α7 Nachr, supplied by OriGene, used in various techniques. Bioz Stars score: 91/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ribobio α7 nachr
    <t>α7</t> <t>nAchR</t> negatively regulates inflammasome activation. (A) LPS-primed peritoneal mouse macrophages from either WT or α7 nAchR knockout (a7 KO) mice were stimulated with ATP in the presence or the absence of acetylcholine for 30 min. (B)
    α7 Nachr, supplied by Ribobio, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Syntaxin α7 nachr
    Codistribution of tSNAREs with <t>α7-nAChR</t> clusters on CG neurons. Freshly dissociated E14 CG neurons were costained with AlexaαBgt for α7-nAChRs ( A, D, G, J ) and antibodies for SNAP-25 ( B ), syntaxin 1 ( E ), SV2 ( H ), or nonimmune serum as a negative control ( K ), and the corresponding pairs of fluorescence images were merged ( C, F, I, L ). Both SNAP-25 and syntaxin 1 codistribute with α7-nAChRs. Similar results were obtained in three additional experiments. Scale bar, 10 μm.
    α7 Nachr, supplied by Syntaxin, used in various techniques. Bioz Stars score: 91/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Pfizer Inc α7 nachr
    Synthesis of <t>α7</t> <t>nAChR</t> ligands. Reagents and conditions: (a) ArCOCH 2- CO 2 Me, i-BuOH, 100 °C, overnight; (b) methyl 2-(cyanomethoxy)benzoate, CS 2 (one drop), 100–110 °C, overnight; (c) (2-cyanophenoxy)acetonitrile, CS 2 (one
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    The Jackson Laboratory α7 nachr knockout mice
    GABAergic synapse formation was impaired in the prefrontal cortex of <t>α7</t> <t>nAChR</t> null mice during late postnatal development and adulthood
    α7 Nachr Knockout Mice, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 93/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abbkine α7 nachr
    Effects of EA on the expression of <t>α7-nAChR</t> (A) Immunofluorescence analysis was performed to determine α7-nAChR expression on Tiabilis anterior muscle 14 days after the procedure. The samples were immunostained with an anti-α7-nAChR-antibody (red, → marks a positive expression). The result shows that α7-nAChR expression are sharply increased and clustered on the muscle membrane of rats in the immobilization group. Representative results from three independent experiments are shown here (scale bar = 50 μm). (B) The Western blot analysis of the α7-nAChR proteins are shown for each groups. Relative intensity of α7-nAChR to GAPDH is shown in the graphs. α7-nAChR significantly increased after the immobilization for 14 days. Electroacupuncture suppressed the expression of α7-nAChR in EA group. All values are expressed as means ± SD (n=6/group). # P
    α7 Nachr, supplied by Abbkine, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Stimulation of α7 nAChR blocks TNF-induced NF-κB activation in BMDMs in vitro and postoperative systemic inflammation

    Journal: Annals of neurology

    Article Title: Resolving postoperative neuroinflammation and cognitive decline

    doi: 10.1002/ana.22664

    Figure Lengend Snippet: Stimulation of α7 nAChR blocks TNF-induced NF-κB activation in BMDMs in vitro and postoperative systemic inflammation

    Article Snippet: PHA 568487 (PHA), a selective agonist of α7 nAChR, was purchased from Tocris Bioscience (Ellisville, MO).

    Techniques: Activation Assay, In Vitro

    Nicotine acts through α7 nAChRs. a The absence of α7 nAChR was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values

    Journal: Respiratory Research

    Article Title: Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors

    doi: 10.1186/s12931-017-0596-8

    Figure Lengend Snippet: Nicotine acts through α7 nAChRs. a The absence of α7 nAChR was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values

    Article Snippet: Blots were incubated with primary polyclonal antibody against either GAPDH (Abcam) (1:5000 dilution), collagen type I (ACRIS, San Diego, CA or Abcam, Cambridge, MA) (1:1000), total and p-Smad (Rockland Immunochemicals, Gilbertsville, PA) (1:2000), total and p-ERK 1 & 2 (Cell Signaling, Beverly, MA) (1:1000), and α7 nAChR (Sigma) (1:500).

    Techniques: Expressing, Mouse Assay, Polymerase Chain Reaction, Western Blot, SDS Page, Nucleic Acid Electrophoresis

    Nicotine Stimulates the Proliferation of Lung Fibroblasts via α7 nAChR-mediated Induction of ERK. a Lung fibroblasts were cultured for up to 72 h after transfection with control (Csi) or α7 nAChR siRNAs (α7si). Silencing of α7 nAChR was confirmed with Western blot (not shown). At the appropriate times, the experiment was halted and live cells counted. Nicotine stimulated cell proliferation at 48 and 72 h, while α7 nAChR siRNA inhibited the nicotine-induced response at 48 and 72 h when compared to nicotine-treated control cells. b Fibroblasts were cultured for up to 72 h with or without nicotine (50 μg/ml) in the presence or absence of PD98059 (MI, 50 μM), an inhibitor of MEK-1. Cell number was determined with the use of a Neubauer hemacytometer along with trypan blue stain. Cell viability was unchanged with treatment (Not Shown). Note that nicotine stimulated fibroblast proliferation at 48 h, but the effect was most noticeable at 72 h. The inhibitor PD98095 alone did not affect the proliferation of cells, but inhibited the stimulatory effect of nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Journal: Respiratory Research

    Article Title: Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors

    doi: 10.1186/s12931-017-0596-8

    Figure Lengend Snippet: Nicotine Stimulates the Proliferation of Lung Fibroblasts via α7 nAChR-mediated Induction of ERK. a Lung fibroblasts were cultured for up to 72 h after transfection with control (Csi) or α7 nAChR siRNAs (α7si). Silencing of α7 nAChR was confirmed with Western blot (not shown). At the appropriate times, the experiment was halted and live cells counted. Nicotine stimulated cell proliferation at 48 and 72 h, while α7 nAChR siRNA inhibited the nicotine-induced response at 48 and 72 h when compared to nicotine-treated control cells. b Fibroblasts were cultured for up to 72 h with or without nicotine (50 μg/ml) in the presence or absence of PD98059 (MI, 50 μM), an inhibitor of MEK-1. Cell number was determined with the use of a Neubauer hemacytometer along with trypan blue stain. Cell viability was unchanged with treatment (Not Shown). Note that nicotine stimulated fibroblast proliferation at 48 h, but the effect was most noticeable at 72 h. The inhibitor PD98095 alone did not affect the proliferation of cells, but inhibited the stimulatory effect of nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Article Snippet: Blots were incubated with primary polyclonal antibody against either GAPDH (Abcam) (1:5000 dilution), collagen type I (ACRIS, San Diego, CA or Abcam, Cambridge, MA) (1:1000), total and p-Smad (Rockland Immunochemicals, Gilbertsville, PA) (1:2000), total and p-ERK 1 & 2 (Cell Signaling, Beverly, MA) (1:1000), and α7 nAChR (Sigma) (1:500).

    Techniques: Cell Culture, Transfection, Western Blot, Staining

    Matrices Derived from Nicotine-treated Fibroblasts and Mice Stimulate IL-1β Expression in Monocytic Cells. a Lung fibroblasts (5x10 4 cells/12 well) were treated with nicotine (50 μg/ml) for 120 h. Fibroblasts were removed by osmotic lysis, the plates were washed thoroughly, and human monocytic U937 cells expressing the human interleukin-1β gene promoter connected to a luciferase reporter gene were overlaid atop the fibroblast-derived matrix. Afterwards, expression of the IL-1β promoter was analyzed by luciferase assay. We found that collagen-containing matrices derived from nicotine-treated fibroblasts stimulated monocytic cells to express the pro-inflammatory cytokine IL-1β. Furthermore, nicotine-treated fibroblast matrix induction of IL-1β was inhibited by anti-α2β1 integrin antibodies. b IL-1β gene transcription was not increased in U937 cells cultured on matrices derived from nicotine-treated α7 nAChR deficient primary lung fibroblast matrix over control. c Fibroblasts pretreated with MG 624, an α7 nAChR antagonist (10 μM), concurrently with nicotine inhibited IL-1β expression without affecting baseline expression. d The nicotine-treated fibroblast matrix IL-1β induction was inhibited by MEK-1 inhibitor PD98059 (50 μM), with PD98059 alone bringing IL-1β expression below baseline. e The lungs of mice exposed to nicotine (100 μg/ml in the drinking water for 8 weeks) were isolated for RNA analysis, which showed an increase in IL-1β gene transcription by RT-PCR. f Lungs from control and nicotine-treated mice were stained by immunohistochemistry for IL-1β. Increased staining was present in mice treated with nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Journal: Respiratory Research

    Article Title: Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors

    doi: 10.1186/s12931-017-0596-8

    Figure Lengend Snippet: Matrices Derived from Nicotine-treated Fibroblasts and Mice Stimulate IL-1β Expression in Monocytic Cells. a Lung fibroblasts (5x10 4 cells/12 well) were treated with nicotine (50 μg/ml) for 120 h. Fibroblasts were removed by osmotic lysis, the plates were washed thoroughly, and human monocytic U937 cells expressing the human interleukin-1β gene promoter connected to a luciferase reporter gene were overlaid atop the fibroblast-derived matrix. Afterwards, expression of the IL-1β promoter was analyzed by luciferase assay. We found that collagen-containing matrices derived from nicotine-treated fibroblasts stimulated monocytic cells to express the pro-inflammatory cytokine IL-1β. Furthermore, nicotine-treated fibroblast matrix induction of IL-1β was inhibited by anti-α2β1 integrin antibodies. b IL-1β gene transcription was not increased in U937 cells cultured on matrices derived from nicotine-treated α7 nAChR deficient primary lung fibroblast matrix over control. c Fibroblasts pretreated with MG 624, an α7 nAChR antagonist (10 μM), concurrently with nicotine inhibited IL-1β expression without affecting baseline expression. d The nicotine-treated fibroblast matrix IL-1β induction was inhibited by MEK-1 inhibitor PD98059 (50 μM), with PD98059 alone bringing IL-1β expression below baseline. e The lungs of mice exposed to nicotine (100 μg/ml in the drinking water for 8 weeks) were isolated for RNA analysis, which showed an increase in IL-1β gene transcription by RT-PCR. f Lungs from control and nicotine-treated mice were stained by immunohistochemistry for IL-1β. Increased staining was present in mice treated with nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Article Snippet: Blots were incubated with primary polyclonal antibody against either GAPDH (Abcam) (1:5000 dilution), collagen type I (ACRIS, San Diego, CA or Abcam, Cambridge, MA) (1:1000), total and p-Smad (Rockland Immunochemicals, Gilbertsville, PA) (1:2000), total and p-ERK 1 & 2 (Cell Signaling, Beverly, MA) (1:1000), and α7 nAChR (Sigma) (1:500).

    Techniques: Derivative Assay, Mouse Assay, Expressing, Lysis, Luciferase, Cell Culture, Isolation, Reverse Transcription Polymerase Chain Reaction, Staining, Immunohistochemistry

    Selective α7-nAChR agonist, PNU-282987, enhances insulin sensitivity through activating STAT3. Western blots in (A) skeletal muscle, (B) visceral adipose and (C) liver in wild type mice after six weeks of saline or PNU-282987 treatment. Data are means ± SE (n = 5–6). * P

    Journal: PLoS ONE

    Article Title: Chronic Exposure to Nicotine Enhances Insulin Sensitivity through ?7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

    doi: 10.1371/journal.pone.0051217

    Figure Lengend Snippet: Selective α7-nAChR agonist, PNU-282987, enhances insulin sensitivity through activating STAT3. Western blots in (A) skeletal muscle, (B) visceral adipose and (C) liver in wild type mice after six weeks of saline or PNU-282987 treatment. Data are means ± SE (n = 5–6). * P

    Article Snippet: Antibodies against α7-nAChR were from Millipore (MA, USA).

    Techniques: Western Blot, Mouse Assay

    Selective α7-nAChR agonist, PNU-282987, enhances insulin sensitivity in normal mice. (A) Weight gain in mice during PNU-282987 treatment. At the end of PNU-282987 treatment, (B) HOMA-IR, (C) insulin tolerance test (ITT) and (D, E) glucose tolerance test (GTT) were performed. ITT was performed in mice 6 h after food removal with insulin challenge at 0.55 IU/kg of body weight (i.p.). GTT was performed in overnight fasted mice with glucose challenge at 2.0 g/kg of body weight (i.p.). Data are means ± SE (n = 5–6). * P

    Journal: PLoS ONE

    Article Title: Chronic Exposure to Nicotine Enhances Insulin Sensitivity through ?7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

    doi: 10.1371/journal.pone.0051217

    Figure Lengend Snippet: Selective α7-nAChR agonist, PNU-282987, enhances insulin sensitivity in normal mice. (A) Weight gain in mice during PNU-282987 treatment. At the end of PNU-282987 treatment, (B) HOMA-IR, (C) insulin tolerance test (ITT) and (D, E) glucose tolerance test (GTT) were performed. ITT was performed in mice 6 h after food removal with insulin challenge at 0.55 IU/kg of body weight (i.p.). GTT was performed in overnight fasted mice with glucose challenge at 2.0 g/kg of body weight (i.p.). Data are means ± SE (n = 5–6). * P

    Article Snippet: Antibodies against α7-nAChR were from Millipore (MA, USA).

    Techniques: Mouse Assay

    α7-nAChR knockout abrogates insulin sensitizing effect of nicotine. (A) Genotype characterization by PCR analysis of tail DNA from offspring derived from heterozygous intercrosses. Expected fragment sizes of the wild-type mice (+/+; 440 bp), heterozygous knockout mice (+/−, 440 bp and 750 bp) and homozygotous knockout mice (−/−; 750 bp) are shown. Only α7-nAChR homozygotous knockout mice were used for chronic treatment. After 6 weeks of saline or nicotine treatment, (B) weight gain, (C, D) basal metabolic parameters and (E, F) insulin sensitivity indexes were evaluated in α7-nAChR −/− mice. Data are means ± SE (n = 5–6). ** P

    Journal: PLoS ONE

    Article Title: Chronic Exposure to Nicotine Enhances Insulin Sensitivity through ?7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

    doi: 10.1371/journal.pone.0051217

    Figure Lengend Snippet: α7-nAChR knockout abrogates insulin sensitizing effect of nicotine. (A) Genotype characterization by PCR analysis of tail DNA from offspring derived from heterozygous intercrosses. Expected fragment sizes of the wild-type mice (+/+; 440 bp), heterozygous knockout mice (+/−, 440 bp and 750 bp) and homozygotous knockout mice (−/−; 750 bp) are shown. Only α7-nAChR homozygotous knockout mice were used for chronic treatment. After 6 weeks of saline or nicotine treatment, (B) weight gain, (C, D) basal metabolic parameters and (E, F) insulin sensitivity indexes were evaluated in α7-nAChR −/− mice. Data are means ± SE (n = 5–6). ** P

    Article Snippet: Antibodies against α7-nAChR were from Millipore (MA, USA).

    Techniques: Knock-Out, Polymerase Chain Reaction, Derivative Assay, Mouse Assay

    Selective α7-nAChR agonist, PNU-282987, enhances insulin sensitivity in AMPKα2 −/− mice. (A) Genotype characterization by PCR analysis of tail DNA from offspring derived from heterozygous intercrosses. Expected fragment sizes of the wild-type mice (+/+; 200 bp), heterozygous knockout mice (+/−, 200 bp and 600 bp) and homozygous knockout mice (−/−; 600 bp) are shown. (B) Weight gain in mice during PNU-282987 treatment. At the end of treatment, (C) HOMA-IR, (D) insulin tolerance test (ITT) and (E, F) glucose tolerance test (GTT) were performed. ITT was performed in mice 6 h after food removal with insulin challenge at 0.55 IU/kg of body weight (i.p.). GTT was performed in overnight fasted mice with glucose challenge at 2.0 g/kg of body weight (i.p.). Data are means ± SE (n = 5–6). # P

    Journal: PLoS ONE

    Article Title: Chronic Exposure to Nicotine Enhances Insulin Sensitivity through ?7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

    doi: 10.1371/journal.pone.0051217

    Figure Lengend Snippet: Selective α7-nAChR agonist, PNU-282987, enhances insulin sensitivity in AMPKα2 −/− mice. (A) Genotype characterization by PCR analysis of tail DNA from offspring derived from heterozygous intercrosses. Expected fragment sizes of the wild-type mice (+/+; 200 bp), heterozygous knockout mice (+/−, 200 bp and 600 bp) and homozygous knockout mice (−/−; 600 bp) are shown. (B) Weight gain in mice during PNU-282987 treatment. At the end of treatment, (C) HOMA-IR, (D) insulin tolerance test (ITT) and (E, F) glucose tolerance test (GTT) were performed. ITT was performed in mice 6 h after food removal with insulin challenge at 0.55 IU/kg of body weight (i.p.). GTT was performed in overnight fasted mice with glucose challenge at 2.0 g/kg of body weight (i.p.). Data are means ± SE (n = 5–6). # P

    Article Snippet: Antibodies against α7-nAChR were from Millipore (MA, USA).

    Techniques: Mouse Assay, Polymerase Chain Reaction, Derivative Assay, Knock-Out

    Blocking peripheral nAChRs except for α7-nAChR by hexamethonium pretreatment has no effect on insulin sensitizing effect of nicotine in normal rats. After 6 weeks of treatment with saline followed by saline or nicotine (Control), or with hexamethonium followed by saline or nicotine (Hex), (A) weight gain, (B, C, D) basal metabolic parameters and (E, F) insulin sensitivity indexes were examined. Data are means ± SE (n = 7–8). * P

    Journal: PLoS ONE

    Article Title: Chronic Exposure to Nicotine Enhances Insulin Sensitivity through ?7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

    doi: 10.1371/journal.pone.0051217

    Figure Lengend Snippet: Blocking peripheral nAChRs except for α7-nAChR by hexamethonium pretreatment has no effect on insulin sensitizing effect of nicotine in normal rats. After 6 weeks of treatment with saline followed by saline or nicotine (Control), or with hexamethonium followed by saline or nicotine (Hex), (A) weight gain, (B, C, D) basal metabolic parameters and (E, F) insulin sensitivity indexes were examined. Data are means ± SE (n = 7–8). * P

    Article Snippet: Antibodies against α7-nAChR were from Millipore (MA, USA).

    Techniques: Blocking Assay

    Nicotine acts through α7 nAChRs. a The absence of α7 nAChR was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values

    Journal: Respiratory Research

    Article Title: Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors

    doi: 10.1186/s12931-017-0596-8

    Figure Lengend Snippet: Nicotine acts through α7 nAChRs. a The absence of α7 nAChR was verified by mRNA and protein expression in the α7KO mice. b α7KO fibroblasts were exposed to nicotine for 24 h and PCR run for collagen type I mRNA expression. Nicotine failed to stimulate collagen type I mRNA expression in α7KO cells. c Nicotine-treated α7KO fibroblasts were subjected to Western blot analysis using anti-collagen type I antibody or GAPDH, followed by secondary goat anti-rabbit IgG (IRDye®). Protein bands were separated by native (collagen type 1) or SDS-PAGE (GAPDH) gel electrophoresis (8%) and quantified by densitometry. Nicotine did not stimulate increased collagen deposition in α7KO fibroblasts. Experiments were repeated at least 3 times. Significance was assessed using p values

    Article Snippet: Polyclonal antibodies against the murine α7 nAChR, and MG 624, an α7 nAChR inhibitor, were purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, California).

    Techniques: Expressing, Mouse Assay, Polymerase Chain Reaction, Western Blot, SDS Page, Nucleic Acid Electrophoresis

    Nicotine Stimulates the Proliferation of Lung Fibroblasts via α7 nAChR-mediated Induction of ERK. a Lung fibroblasts were cultured for up to 72 h after transfection with control (Csi) or α7 nAChR siRNAs (α7si). Silencing of α7 nAChR was confirmed with Western blot (not shown). At the appropriate times, the experiment was halted and live cells counted. Nicotine stimulated cell proliferation at 48 and 72 h, while α7 nAChR siRNA inhibited the nicotine-induced response at 48 and 72 h when compared to nicotine-treated control cells. b Fibroblasts were cultured for up to 72 h with or without nicotine (50 μg/ml) in the presence or absence of PD98059 (MI, 50 μM), an inhibitor of MEK-1. Cell number was determined with the use of a Neubauer hemacytometer along with trypan blue stain. Cell viability was unchanged with treatment (Not Shown). Note that nicotine stimulated fibroblast proliferation at 48 h, but the effect was most noticeable at 72 h. The inhibitor PD98095 alone did not affect the proliferation of cells, but inhibited the stimulatory effect of nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Journal: Respiratory Research

    Article Title: Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors

    doi: 10.1186/s12931-017-0596-8

    Figure Lengend Snippet: Nicotine Stimulates the Proliferation of Lung Fibroblasts via α7 nAChR-mediated Induction of ERK. a Lung fibroblasts were cultured for up to 72 h after transfection with control (Csi) or α7 nAChR siRNAs (α7si). Silencing of α7 nAChR was confirmed with Western blot (not shown). At the appropriate times, the experiment was halted and live cells counted. Nicotine stimulated cell proliferation at 48 and 72 h, while α7 nAChR siRNA inhibited the nicotine-induced response at 48 and 72 h when compared to nicotine-treated control cells. b Fibroblasts were cultured for up to 72 h with or without nicotine (50 μg/ml) in the presence or absence of PD98059 (MI, 50 μM), an inhibitor of MEK-1. Cell number was determined with the use of a Neubauer hemacytometer along with trypan blue stain. Cell viability was unchanged with treatment (Not Shown). Note that nicotine stimulated fibroblast proliferation at 48 h, but the effect was most noticeable at 72 h. The inhibitor PD98095 alone did not affect the proliferation of cells, but inhibited the stimulatory effect of nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Article Snippet: Polyclonal antibodies against the murine α7 nAChR, and MG 624, an α7 nAChR inhibitor, were purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, California).

    Techniques: Cell Culture, Transfection, Western Blot, Staining

    Matrices Derived from Nicotine-treated Fibroblasts and Mice Stimulate IL-1β Expression in Monocytic Cells. a Lung fibroblasts (5x10 4 cells/12 well) were treated with nicotine (50 μg/ml) for 120 h. Fibroblasts were removed by osmotic lysis, the plates were washed thoroughly, and human monocytic U937 cells expressing the human interleukin-1β gene promoter connected to a luciferase reporter gene were overlaid atop the fibroblast-derived matrix. Afterwards, expression of the IL-1β promoter was analyzed by luciferase assay. We found that collagen-containing matrices derived from nicotine-treated fibroblasts stimulated monocytic cells to express the pro-inflammatory cytokine IL-1β. Furthermore, nicotine-treated fibroblast matrix induction of IL-1β was inhibited by anti-α2β1 integrin antibodies. b IL-1β gene transcription was not increased in U937 cells cultured on matrices derived from nicotine-treated α7 nAChR deficient primary lung fibroblast matrix over control. c Fibroblasts pretreated with MG 624, an α7 nAChR antagonist (10 μM), concurrently with nicotine inhibited IL-1β expression without affecting baseline expression. d The nicotine-treated fibroblast matrix IL-1β induction was inhibited by MEK-1 inhibitor PD98059 (50 μM), with PD98059 alone bringing IL-1β expression below baseline. e The lungs of mice exposed to nicotine (100 μg/ml in the drinking water for 8 weeks) were isolated for RNA analysis, which showed an increase in IL-1β gene transcription by RT-PCR. f Lungs from control and nicotine-treated mice were stained by immunohistochemistry for IL-1β. Increased staining was present in mice treated with nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Journal: Respiratory Research

    Article Title: Nicotine stimulates collagen type I expression in lung via α7 nicotinic acetylcholine receptors

    doi: 10.1186/s12931-017-0596-8

    Figure Lengend Snippet: Matrices Derived from Nicotine-treated Fibroblasts and Mice Stimulate IL-1β Expression in Monocytic Cells. a Lung fibroblasts (5x10 4 cells/12 well) were treated with nicotine (50 μg/ml) for 120 h. Fibroblasts were removed by osmotic lysis, the plates were washed thoroughly, and human monocytic U937 cells expressing the human interleukin-1β gene promoter connected to a luciferase reporter gene were overlaid atop the fibroblast-derived matrix. Afterwards, expression of the IL-1β promoter was analyzed by luciferase assay. We found that collagen-containing matrices derived from nicotine-treated fibroblasts stimulated monocytic cells to express the pro-inflammatory cytokine IL-1β. Furthermore, nicotine-treated fibroblast matrix induction of IL-1β was inhibited by anti-α2β1 integrin antibodies. b IL-1β gene transcription was not increased in U937 cells cultured on matrices derived from nicotine-treated α7 nAChR deficient primary lung fibroblast matrix over control. c Fibroblasts pretreated with MG 624, an α7 nAChR antagonist (10 μM), concurrently with nicotine inhibited IL-1β expression without affecting baseline expression. d The nicotine-treated fibroblast matrix IL-1β induction was inhibited by MEK-1 inhibitor PD98059 (50 μM), with PD98059 alone bringing IL-1β expression below baseline. e The lungs of mice exposed to nicotine (100 μg/ml in the drinking water for 8 weeks) were isolated for RNA analysis, which showed an increase in IL-1β gene transcription by RT-PCR. f Lungs from control and nicotine-treated mice were stained by immunohistochemistry for IL-1β. Increased staining was present in mice treated with nicotine. Experiments were repeated at least 3 times. Significance was assessed using p values

    Article Snippet: Polyclonal antibodies against the murine α7 nAChR, and MG 624, an α7 nAChR inhibitor, were purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, California).

    Techniques: Derivative Assay, Mouse Assay, Expressing, Lysis, Luciferase, Cell Culture, Isolation, Reverse Transcription Polymerase Chain Reaction, Staining, Immunohistochemistry

    Nicotinic receptors on mouse BAL cells . (A) RT-PCR, agarose gel electrophoresis. Mouse BAL cells consistently express mRNAs coding for α9, β2 and β4 subunits. Subunit α10 shows an interindividual expression pattern. The mRNA for α7 subunit was not found in BAL preparations, although it was easily detectable in brain homogenate, serving as a positive control. M = DNA marker, H 2 O = water control (B) Ratiometric [Ca 2+ ] i recordings. Mouse BAL cells isolated from C57BL6N, α7 nAChR knockout (α7 -/- ) and littermate control animals (α7 +/+ ) were stimulated with ATP (10 -4 M) in the presence or absence (Hepes) of nicotine (10 -4 M). Peak increases shown as mean ± SEM; cells taken from 6-9 coverslips for each experimental setup, p-values calculated by Mann-Whitney test.

    Journal: Respiratory Research

    Article Title: Nicotinic receptors on rat alveolar macrophages dampen ATP-induced increase in cytosolic calcium concentration

    doi: 10.1186/1465-9921-11-133

    Figure Lengend Snippet: Nicotinic receptors on mouse BAL cells . (A) RT-PCR, agarose gel electrophoresis. Mouse BAL cells consistently express mRNAs coding for α9, β2 and β4 subunits. Subunit α10 shows an interindividual expression pattern. The mRNA for α7 subunit was not found in BAL preparations, although it was easily detectable in brain homogenate, serving as a positive control. M = DNA marker, H 2 O = water control (B) Ratiometric [Ca 2+ ] i recordings. Mouse BAL cells isolated from C57BL6N, α7 nAChR knockout (α7 -/- ) and littermate control animals (α7 +/+ ) were stimulated with ATP (10 -4 M) in the presence or absence (Hepes) of nicotine (10 -4 M). Peak increases shown as mean ± SEM; cells taken from 6-9 coverslips for each experimental setup, p-values calculated by Mann-Whitney test.

    Article Snippet: Mice deficient for the α7 nAChR subunit were obtained from Jackson Laboratory (Bar Harbor, USA) and bred in SPF conditions by the local animal breeding facility using heterozygotes as breeders.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Expressing, Positive Control, Marker, Isolation, Knock-Out, MANN-WHITNEY

    Double-labeling immunofluorescence demonstrating the presence of the nAChR subunits α5, α9, α10 and β2 in ED1-positive BAL cells . A punctate fluorescence pattern for the α5 and α9 nAChR subunits was found in a subset of AM (inserts) . Negative results were noted for α3 and α7 subunits in ED1-positive cells, despite occasional occurrence of α3 subunit immunoreactive ED1-negative cells (arrow) . Bar: 20 μm, 10 μm in inserts.

    Journal: Respiratory Research

    Article Title: Nicotinic receptors on rat alveolar macrophages dampen ATP-induced increase in cytosolic calcium concentration

    doi: 10.1186/1465-9921-11-133

    Figure Lengend Snippet: Double-labeling immunofluorescence demonstrating the presence of the nAChR subunits α5, α9, α10 and β2 in ED1-positive BAL cells . A punctate fluorescence pattern for the α5 and α9 nAChR subunits was found in a subset of AM (inserts) . Negative results were noted for α3 and α7 subunits in ED1-positive cells, despite occasional occurrence of α3 subunit immunoreactive ED1-negative cells (arrow) . Bar: 20 μm, 10 μm in inserts.

    Article Snippet: Mice deficient for the α7 nAChR subunit were obtained from Jackson Laboratory (Bar Harbor, USA) and bred in SPF conditions by the local animal breeding facility using heterozygotes as breeders.

    Techniques: Labeling, Immunofluorescence, Fluorescence

    Immunoblots . No α7 subunit-immunolabeling is present in BAL samples, while the antibody mAb 306 recognizes a single 50 kDa protein band in protein extracts from rat brain. Affinity purified polyclonal antibodies to α10 nAChR label a protein band at 67 kDa in BAL cells and rat skin samples. In BAL cells, additional bands at 110-120 kDa are immunolabeled.

    Journal: Respiratory Research

    Article Title: Nicotinic receptors on rat alveolar macrophages dampen ATP-induced increase in cytosolic calcium concentration

    doi: 10.1186/1465-9921-11-133

    Figure Lengend Snippet: Immunoblots . No α7 subunit-immunolabeling is present in BAL samples, while the antibody mAb 306 recognizes a single 50 kDa protein band in protein extracts from rat brain. Affinity purified polyclonal antibodies to α10 nAChR label a protein band at 67 kDa in BAL cells and rat skin samples. In BAL cells, additional bands at 110-120 kDa are immunolabeled.

    Article Snippet: Mice deficient for the α7 nAChR subunit were obtained from Jackson Laboratory (Bar Harbor, USA) and bred in SPF conditions by the local animal breeding facility using heterozygotes as breeders.

    Techniques: Western Blot, Immunolabeling, Affinity Purification

    RT-PCR analysis of nAChR subunits in BAL cells, which consistently express mRNA coding for α9, α10, β1 and β2 subunits . Subunit α5 shows an interindividual expression pattern. The mRNAs coding for α1, α4, α6, α7 and β3 subunits are absent. Positive controls were run on DRG (α2-α10), lung (β2-4), and skeletal muscle (α1 and β1). Negative controls were done without RT.

    Journal: Respiratory Research

    Article Title: Nicotinic receptors on rat alveolar macrophages dampen ATP-induced increase in cytosolic calcium concentration

    doi: 10.1186/1465-9921-11-133

    Figure Lengend Snippet: RT-PCR analysis of nAChR subunits in BAL cells, which consistently express mRNA coding for α9, α10, β1 and β2 subunits . Subunit α5 shows an interindividual expression pattern. The mRNAs coding for α1, α4, α6, α7 and β3 subunits are absent. Positive controls were run on DRG (α2-α10), lung (β2-4), and skeletal muscle (α1 and β1). Negative controls were done without RT.

    Article Snippet: Mice deficient for the α7 nAChR subunit were obtained from Jackson Laboratory (Bar Harbor, USA) and bred in SPF conditions by the local animal breeding facility using heterozygotes as breeders.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing

    Increased spine density in the NAc of α7 nAChR KO mice. ( a ) CA1, CA3, DG from hippocampus. ( b ) Prelimbic and infralimbic regions of medial prefrontal cortex (mPFC). ( c ) Sell and core regions of NAc. Data represent the mean ± S.E.M. (n = 5). *P

    Journal: Scientific Reports

    Article Title: Depression-like phenotype by deletion of α7 nicotinic acetylcholine receptor: Role of BDNF-TrkB in nucleus accumbens

    doi: 10.1038/srep36705

    Figure Lengend Snippet: Increased spine density in the NAc of α7 nAChR KO mice. ( a ) CA1, CA3, DG from hippocampus. ( b ) Prelimbic and infralimbic regions of medial prefrontal cortex (mPFC). ( c ) Sell and core regions of NAc. Data represent the mean ± S.E.M. (n = 5). *P

    Article Snippet: Animals Mice deficient for the α7 nAChR (C57BL/6 background) were purchased from The Jackson Laboratory (Bar Harbor, ME).

    Techniques: Mouse Assay

    Increased BDNF-TrkB signaling in the NAc of α7 nAChR KO mice. ( a , b ): Levels of proBDNF and BDNF in the CA1, CA3, DG, PFC, and NAc. Data represent the mean ± S.E.M. (n = 5 or 6). ( c ): The ratio of phosphor-TrkB to total TrkB. Data represent the mean ± S.E.M. (n = 6). ( d , e ): Levels of GluA1 and PSD-95 in the CA1, CA3, DG, PFC, and NAc. Data represent the mean ± S.E.M. (n = 5 or 6). *P

    Journal: Scientific Reports

    Article Title: Depression-like phenotype by deletion of α7 nicotinic acetylcholine receptor: Role of BDNF-TrkB in nucleus accumbens

    doi: 10.1038/srep36705

    Figure Lengend Snippet: Increased BDNF-TrkB signaling in the NAc of α7 nAChR KO mice. ( a , b ): Levels of proBDNF and BDNF in the CA1, CA3, DG, PFC, and NAc. Data represent the mean ± S.E.M. (n = 5 or 6). ( c ): The ratio of phosphor-TrkB to total TrkB. Data represent the mean ± S.E.M. (n = 6). ( d , e ): Levels of GluA1 and PSD-95 in the CA1, CA3, DG, PFC, and NAc. Data represent the mean ± S.E.M. (n = 5 or 6). *P

    Article Snippet: Animals Mice deficient for the α7 nAChR (C57BL/6 background) were purchased from The Jackson Laboratory (Bar Harbor, ME).

    Techniques: Mouse Assay

    Effects of 7,8-DHF and fluoxetine in α7 nAChR KO mice. ( a , e ): locomotion, ( b , f ): TST, ( c , g ): FST, ( d , h ): SPT): The TrkB agonist 7,8-DHF and SSRI fluoxetine did not show antidepressant effects in α7 nAChR KO mice. Data represent the mean ± S.E.M. (n = 12–14). *P

    Journal: Scientific Reports

    Article Title: Depression-like phenotype by deletion of α7 nicotinic acetylcholine receptor: Role of BDNF-TrkB in nucleus accumbens

    doi: 10.1038/srep36705

    Figure Lengend Snippet: Effects of 7,8-DHF and fluoxetine in α7 nAChR KO mice. ( a , e ): locomotion, ( b , f ): TST, ( c , g ): FST, ( d , h ): SPT): The TrkB agonist 7,8-DHF and SSRI fluoxetine did not show antidepressant effects in α7 nAChR KO mice. Data represent the mean ± S.E.M. (n = 12–14). *P

    Article Snippet: Animals Mice deficient for the α7 nAChR (C57BL/6 background) were purchased from The Jackson Laboratory (Bar Harbor, ME).

    Techniques: Mouse Assay, Single-particle Tracking

    Depression-like phenotypes, and inflammation in α7 nAChR KO mice. ( a ) locomotion, ( b ): tail-suspension test (TST), ( c ): forced swimming test (FST), ( d ): 1% sucrose preference test (SPT). Data represent the mean ± S.E.M. (n = 8 or 9). ( e ): Dexamethasone (DEX) suppression test. Data represent the mean ± S.E.M. (n = 8 or 9). ( f ): Serum levels of TNF-α. Data represent the mean ± S.E.M. (n = 11). ( g ): Serum levels of IL-1β. Data represent the mean ± S.E.M. (n = 7 or 8). ( h ): Serum levels of IL-6. Data represent the mean ± S.E.M. (n = 12 or 13). *P

    Journal: Scientific Reports

    Article Title: Depression-like phenotype by deletion of α7 nicotinic acetylcholine receptor: Role of BDNF-TrkB in nucleus accumbens

    doi: 10.1038/srep36705

    Figure Lengend Snippet: Depression-like phenotypes, and inflammation in α7 nAChR KO mice. ( a ) locomotion, ( b ): tail-suspension test (TST), ( c ): forced swimming test (FST), ( d ): 1% sucrose preference test (SPT). Data represent the mean ± S.E.M. (n = 8 or 9). ( e ): Dexamethasone (DEX) suppression test. Data represent the mean ± S.E.M. (n = 8 or 9). ( f ): Serum levels of TNF-α. Data represent the mean ± S.E.M. (n = 11). ( g ): Serum levels of IL-1β. Data represent the mean ± S.E.M. (n = 7 or 8). ( h ): Serum levels of IL-6. Data represent the mean ± S.E.M. (n = 12 or 13). *P

    Article Snippet: Animals Mice deficient for the α7 nAChR (C57BL/6 background) were purchased from The Jackson Laboratory (Bar Harbor, ME).

    Techniques: Mouse Assay, Single-particle Tracking

    Intracellular calcium, CaMKII and MAPK are required for α7-nAChR-mediated depression of GABA A receptor responses in CG neurons A , paired traces as in showing GABA-induced responses 1 min before and 2 s after applying nicotine for 3 s using

    Journal:

    Article Title: Reversible inhibition of GABAA receptors by ?7-containing nicotinic receptors on the vertebrate postsynaptic neurons

    doi: 10.1113/jphysiol.2006.124578

    Figure Lengend Snippet: Intracellular calcium, CaMKII and MAPK are required for α7-nAChR-mediated depression of GABA A receptor responses in CG neurons A , paired traces as in showing GABA-induced responses 1 min before and 2 s after applying nicotine for 3 s using

    Article Snippet: C57/BL6 mice heterozygous for knockout of the α7-nAChR gene were purchased from Jackson Laboratories (Bar Harbor, ME, USA) and used to establish a colony.

    Techniques:

    Nicotinic activation of α7-nAChR depresses GABAergic IPSCs in mouse hippocampal CA1 interneurons A , diagram showing electrode positions to elicit IPSCs by electrical stimulation in SR (Stim) while recording from an SR interneuron (Record). Nicotine

    Journal:

    Article Title: Reversible inhibition of GABAA receptors by ?7-containing nicotinic receptors on the vertebrate postsynaptic neurons

    doi: 10.1113/jphysiol.2006.124578

    Figure Lengend Snippet: Nicotinic activation of α7-nAChR depresses GABAergic IPSCs in mouse hippocampal CA1 interneurons A , diagram showing electrode positions to elicit IPSCs by electrical stimulation in SR (Stim) while recording from an SR interneuron (Record). Nicotine

    Article Snippet: C57/BL6 mice heterozygous for knockout of the α7-nAChR gene were purchased from Jackson Laboratories (Bar Harbor, ME, USA) and used to establish a colony.

    Techniques: Activation Assay

    Involvements of α7 nAChR, and PI3K, JNK and PKC pathways in the induction of EP4 by nicotine ( A ) Acetylcholine increased the expression of EP4 induced by nicotine in dose-dependent in A549 cells. ( B ) Acetylcholinesterase decreased the expression of EP4 induced by nicotine in dose-dependent in A549 cells. ( C ) a-bungarotoxin of a a7 nAChR blocker, not dihydro-β-erythroidine of a α4 nAChR inhibitor, decreased the expression of EP4 induced by nicotine in A549 cells. ( D ) α7 nAChR siRNA (100 nM) decreased the expression of EP4 induced by nicotine in A549 cells. ( E ) a-bungarotoxin, a a7 nAChR blocker, decreased the proliferation induced by nicotine in A549 cells and H1838 cells. ( F ) The specific inhibitors of PI3-K (wortmannin, 1 μM), JNK (SP600125, 20 μM) reduced expression of EP4 induced by nicotine in A549 cells. ( G ) The specific inhibitors of ERK (PD98095, 20 μM), not P38 MAPK (SB239063, 10 μM) had a minor effect on reduction of EP4 induced by nicotine in A549 cells. ( H ) The specific inhibitors of PKC (calphostin C, 0.5 μM), not PKA (H89, 10 μM) reduced expression of EP4 induced by nicotine in A549 cells. GAPDH served as internal control for normalization purposes.

    Journal: Oncotarget

    Article Title: Nicotine induces EP4 receptor expression in lung carcinoma cells by acting on AP-2α: The intersection between cholinergic and prostanoid signaling

    doi: 10.18632/oncotarget.18023

    Figure Lengend Snippet: Involvements of α7 nAChR, and PI3K, JNK and PKC pathways in the induction of EP4 by nicotine ( A ) Acetylcholine increased the expression of EP4 induced by nicotine in dose-dependent in A549 cells. ( B ) Acetylcholinesterase decreased the expression of EP4 induced by nicotine in dose-dependent in A549 cells. ( C ) a-bungarotoxin of a a7 nAChR blocker, not dihydro-β-erythroidine of a α4 nAChR inhibitor, decreased the expression of EP4 induced by nicotine in A549 cells. ( D ) α7 nAChR siRNA (100 nM) decreased the expression of EP4 induced by nicotine in A549 cells. ( E ) a-bungarotoxin, a a7 nAChR blocker, decreased the proliferation induced by nicotine in A549 cells and H1838 cells. ( F ) The specific inhibitors of PI3-K (wortmannin, 1 μM), JNK (SP600125, 20 μM) reduced expression of EP4 induced by nicotine in A549 cells. ( G ) The specific inhibitors of ERK (PD98095, 20 μM), not P38 MAPK (SB239063, 10 μM) had a minor effect on reduction of EP4 induced by nicotine in A549 cells. ( H ) The specific inhibitors of PKC (calphostin C, 0.5 μM), not PKA (H89, 10 μM) reduced expression of EP4 induced by nicotine in A549 cells. GAPDH served as internal control for normalization purposes.

    Article Snippet: The α7 nAChR (sc-42532), EP4 (sc-40173) and control (sc-37007) siRNAs, and polyclonal antibodies against AP-2α were purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Expressing

    Effects of oral choline treatment on the gene and protein expression levels, respectively, of α7 nAChR (A and B), HIF-1α (C and D), and VEGF (E and F) in the ischemic cerebral cortex. Mean±SEM. n =3. b P

    Journal: Acta Pharmacologica Sinica

    Article Title: Brain protection against ischemic stroke using choline as a new molecular bypass treatment

    doi: 10.1038/aps.2015.104

    Figure Lengend Snippet: Effects of oral choline treatment on the gene and protein expression levels, respectively, of α7 nAChR (A and B), HIF-1α (C and D), and VEGF (E and F) in the ischemic cerebral cortex. Mean±SEM. n =3. b P

    Article Snippet: Fifty micrograms of protein was separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), transferred from the gel to a polyvinylidene fluoride (PVDF) membrane, and stained using the following primary antibodies prior to incubation with a secondary antibody: anti-α7 nAChR, (1:1000; Abcam, Boston, MA, USA), anti-HIF-1α (1:500, Novus, Cambridge, UK), and anti-VEGF (1:500; Santa Cruz, Dallas, TX, USA).

    Techniques: Expressing

    Antagonists to α7-nAChR abrogated the proangiogenic activity of nicotine in HRMECs. ( A ) Matrigel duplex assays demonstrated that the treatment of HRMECs with 1 μM of the α7-nAChR antagonists, α-BT, α-CT, or MLA, significantly suppressed the proangiogenic activity of nicotine. ( B ) Rat retinal explant assays showed that nicotine-induced angiogenic sprouting was abrogated by 1 μM of α-CT ( bottom left ) and 1 μM of MLA ( bottom right ). ( C ) ELISA assays indicated that treatment of HRMECs with 1 μM of the α7-nAChR antagonists, α-BT, α-CT, or MLA, reduced nicotine-induced secretion of MMP-2 and -9. MMP-13 levels were unaffected by nicotine and the α7-nAChR antagonists.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: The ?7-nicotinic Acetylcholine Receptor and MMP-2/-9 Pathway Mediate the Proangiogenic Effect of Nicotine in Human Retinal Endothelial Cells

    doi: 10.1167/iovs.10-5461

    Figure Lengend Snippet: Antagonists to α7-nAChR abrogated the proangiogenic activity of nicotine in HRMECs. ( A ) Matrigel duplex assays demonstrated that the treatment of HRMECs with 1 μM of the α7-nAChR antagonists, α-BT, α-CT, or MLA, significantly suppressed the proangiogenic activity of nicotine. ( B ) Rat retinal explant assays showed that nicotine-induced angiogenic sprouting was abrogated by 1 μM of α-CT ( bottom left ) and 1 μM of MLA ( bottom right ). ( C ) ELISA assays indicated that treatment of HRMECs with 1 μM of the α7-nAChR antagonists, α-BT, α-CT, or MLA, reduced nicotine-induced secretion of MMP-2 and -9. MMP-13 levels were unaffected by nicotine and the α7-nAChR antagonists.

    Article Snippet: Polyclonal α3-, α4- and α7-nAChR antibodies (Abcam, Cambridge, MA), β2- and β3-nAChR antibodies (Santa Cruz Biotechnologies, Santa Cruz, CA), and GAPDH antibody (Trevigen, Inc., Gaithersburg, MD) were used for the immunoblot experiments., The results of the Western blot assays were quantitated by densitometry (Gel Documentation System, with Quantity One 4.5.2 analysis software; Bio-Rad, Hercules, CA).

    Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay

    A highly simplified summary of the pathways underlying the proangiogenic activity of nicotine in HRMECs. Nicotine binds to high-affinity α7-nAChRs on HRMECs to stimulate the production of MMP-2 and -9 and inhibit levels of TIMP-1 and -2. Both of these processes eventually promote retinal angiogenesis. Another signaling pathway induced by nicotine in HRMECs involves activation of phospholipase A2. Nicotine can also increase the recruitment of endothelial progenitor cells to stimulate neovascularization in the retina. The pathways which connect α7-nAChRs to these downstream signaling proteins are unknown, but they probably involve the secretion of growth factors like bFGF or VEGF in response to nicotine treatment. Taken together, α7-nAChR antagonists could be useful for attenuating the proangiogenic activity of nicotine in retinal endothelial cells.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: The ?7-nicotinic Acetylcholine Receptor and MMP-2/-9 Pathway Mediate the Proangiogenic Effect of Nicotine in Human Retinal Endothelial Cells

    doi: 10.1167/iovs.10-5461

    Figure Lengend Snippet: A highly simplified summary of the pathways underlying the proangiogenic activity of nicotine in HRMECs. Nicotine binds to high-affinity α7-nAChRs on HRMECs to stimulate the production of MMP-2 and -9 and inhibit levels of TIMP-1 and -2. Both of these processes eventually promote retinal angiogenesis. Another signaling pathway induced by nicotine in HRMECs involves activation of phospholipase A2. Nicotine can also increase the recruitment of endothelial progenitor cells to stimulate neovascularization in the retina. The pathways which connect α7-nAChRs to these downstream signaling proteins are unknown, but they probably involve the secretion of growth factors like bFGF or VEGF in response to nicotine treatment. Taken together, α7-nAChR antagonists could be useful for attenuating the proangiogenic activity of nicotine in retinal endothelial cells.

    Article Snippet: Polyclonal α3-, α4- and α7-nAChR antibodies (Abcam, Cambridge, MA), β2- and β3-nAChR antibodies (Santa Cruz Biotechnologies, Santa Cruz, CA), and GAPDH antibody (Trevigen, Inc., Gaithersburg, MD) were used for the immunoblot experiments., The results of the Western blot assays were quantitated by densitometry (Gel Documentation System, with Quantity One 4.5.2 analysis software; Bio-Rad, Hercules, CA).

    Techniques: Activity Assay, Activation Assay

    The α7-nAChR mediated the proangiogenic effect of nicotine in HRMECs. ( A ) Matrigel duplex assays indicated that the transfection of α7-nAChR-siRNA significantly attenuated nicotine-induced angiogenesis, whereas a nontargeting control-siRNA did not have any effect on the proangiogenic effects of nicotine. Most interestingly, siRNA corresponding to the closely related α3-nAChR had no influence on nicotine-induced angiogenesis, as measured by the Matrigel duplex assay. ( B ) Western blot analysis showed that both α7-nAChR and α3-nAChR levels were suppressed on siRNA transfection ( top and middle ). Most importantly, the transfection of α7-nAChR-siRNA had no effect on the expression of α3-nAChR ( top panel , lane 4 ) in HRMECs and vice versa ( middle , lane 3 ). GAPDH was used as the loading control for the Western blot experiments, and the results were quantitated by densitometric analysis. ( C ) ELISA demonstrated that suppression of α7-nAChR levels by siRNA methodology ablated nicotine-induced secretion of MMP-2 and -9. However, the transfection of α3-nAChR-siRNA and nontargeting control-siRNA had no effect on nicotine-induced MMP-2 and -9 levels. MMP-13 levels were unaffected by nicotine. Values indicated by the same letter are not statistically significant.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: The ?7-nicotinic Acetylcholine Receptor and MMP-2/-9 Pathway Mediate the Proangiogenic Effect of Nicotine in Human Retinal Endothelial Cells

    doi: 10.1167/iovs.10-5461

    Figure Lengend Snippet: The α7-nAChR mediated the proangiogenic effect of nicotine in HRMECs. ( A ) Matrigel duplex assays indicated that the transfection of α7-nAChR-siRNA significantly attenuated nicotine-induced angiogenesis, whereas a nontargeting control-siRNA did not have any effect on the proangiogenic effects of nicotine. Most interestingly, siRNA corresponding to the closely related α3-nAChR had no influence on nicotine-induced angiogenesis, as measured by the Matrigel duplex assay. ( B ) Western blot analysis showed that both α7-nAChR and α3-nAChR levels were suppressed on siRNA transfection ( top and middle ). Most importantly, the transfection of α7-nAChR-siRNA had no effect on the expression of α3-nAChR ( top panel , lane 4 ) in HRMECs and vice versa ( middle , lane 3 ). GAPDH was used as the loading control for the Western blot experiments, and the results were quantitated by densitometric analysis. ( C ) ELISA demonstrated that suppression of α7-nAChR levels by siRNA methodology ablated nicotine-induced secretion of MMP-2 and -9. However, the transfection of α3-nAChR-siRNA and nontargeting control-siRNA had no effect on nicotine-induced MMP-2 and -9 levels. MMP-13 levels were unaffected by nicotine. Values indicated by the same letter are not statistically significant.

    Article Snippet: Polyclonal α3-, α4- and α7-nAChR antibodies (Abcam, Cambridge, MA), β2- and β3-nAChR antibodies (Santa Cruz Biotechnologies, Santa Cruz, CA), and GAPDH antibody (Trevigen, Inc., Gaithersburg, MD) were used for the immunoblot experiments., The results of the Western blot assays were quantitated by densitometry (Gel Documentation System, with Quantity One 4.5.2 analysis software; Bio-Rad, Hercules, CA).

    Techniques: Transfection, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

    Nicotine up-regulates Prx1, α3 nAChR and α7 nAChR, enhances EMT, and promotes invasion and migration in SCC15 cells ( A ) mRNA expression of Prx1, α3 nAChR, α7 nAChR, E-cadherin, vimentin and Snail in control and nicotine-treated SCC15 cells; ( B ) representative blots from one of three separate experiments for the protein expression of Prx1, α3 nAChR, α7 nAChR, E-cadherin, vimentin and Snail in control and nicotine-treated SCC15 cells; ( C ) images of invading control and nicotine-treated SCC15 cells detected by Matrigel invasion assay (upper panel) and statistical analysis (lower panel); and ( D ) wound healing assay to examine the effect of nicotine on SCC15 cell mobility. The values are expressed as the mean ± SE. * P

    Journal: Oncotarget

    Article Title: Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis

    doi: 10.18632/oncotarget.9705

    Figure Lengend Snippet: Nicotine up-regulates Prx1, α3 nAChR and α7 nAChR, enhances EMT, and promotes invasion and migration in SCC15 cells ( A ) mRNA expression of Prx1, α3 nAChR, α7 nAChR, E-cadherin, vimentin and Snail in control and nicotine-treated SCC15 cells; ( B ) representative blots from one of three separate experiments for the protein expression of Prx1, α3 nAChR, α7 nAChR, E-cadherin, vimentin and Snail in control and nicotine-treated SCC15 cells; ( C ) images of invading control and nicotine-treated SCC15 cells detected by Matrigel invasion assay (upper panel) and statistical analysis (lower panel); and ( D ) wound healing assay to examine the effect of nicotine on SCC15 cell mobility. The values are expressed as the mean ± SE. * P

    Article Snippet: The blots were incubated with primary antibody for Prx1, α3 nAChR, α7 nAChR, Snail (Abcam, USA), E-cadherin (Cell Signalling Technology, USA), vimentin (Bioss, China), IκBα, p-IκBα, p-NFκB p65 (Cell Signalling Technology, USA), or GAPDH (Sigma, USA).

    Techniques: Migration, Expressing, Invasion Assay, Wound Healing Assay

    The summary model is depicted by which nicotine binds to α7-nAChRs to activate PI3/AKT signaling, thereby upregulating SNCG expression, and this effect was suppressed when α7-nAChR was knocked down or inhibited

    Journal: Cancer Cell International

    Article Title: Gamma synuclein is a novel nicotine responsive protein in oral cancer malignancy

    doi: 10.1186/s12935-020-01401-w

    Figure Lengend Snippet: The summary model is depicted by which nicotine binds to α7-nAChRs to activate PI3/AKT signaling, thereby upregulating SNCG expression, and this effect was suppressed when α7-nAChR was knocked down or inhibited

    Article Snippet: An anti-GAPDH antibody (Cell Signaling, Danvers, MA, USA), anti-fibronectin antibody (Abcam, Cambridge, England, UK), anti-vimentin antibody (cell signaling), anti-E-cadherin antibody (BD Biosciences, Franklin Lakes, NJ, USA), anti-ZO-1 antibody (BD Biosciences), anti-PCNA antibody (Cell Signaling), anti-protein kinase B (AKT) antibody (Cell Signaling), anti-phospho-AKT (P-AKT) antibody (Cell Signaling), anti-α7-nAChR antibody (Abcam), and anti-SNCG antibody (Cell Signaling) were used for probing.

    Techniques: Expressing

    α7-nAChR expression level was abundant in YD8 and OEC-M1 cells. a The mRNA expression of the nAChR subunits in YD8 and OEC-M1 oral cancer cells. The α7-nAChR expression level was measured by b western blot, c PCR analysis in YD8 and OEC-M1 cells. Data represent mean ± SD of 3 independent experiments

    Journal: Cancer Cell International

    Article Title: Gamma synuclein is a novel nicotine responsive protein in oral cancer malignancy

    doi: 10.1186/s12935-020-01401-w

    Figure Lengend Snippet: α7-nAChR expression level was abundant in YD8 and OEC-M1 cells. a The mRNA expression of the nAChR subunits in YD8 and OEC-M1 oral cancer cells. The α7-nAChR expression level was measured by b western blot, c PCR analysis in YD8 and OEC-M1 cells. Data represent mean ± SD of 3 independent experiments

    Article Snippet: An anti-GAPDH antibody (Cell Signaling, Danvers, MA, USA), anti-fibronectin antibody (Abcam, Cambridge, England, UK), anti-vimentin antibody (cell signaling), anti-E-cadherin antibody (BD Biosciences, Franklin Lakes, NJ, USA), anti-ZO-1 antibody (BD Biosciences), anti-PCNA antibody (Cell Signaling), anti-protein kinase B (AKT) antibody (Cell Signaling), anti-phospho-AKT (P-AKT) antibody (Cell Signaling), anti-α7-nAChR antibody (Abcam), and anti-SNCG antibody (Cell Signaling) were used for probing.

    Techniques: Expressing, Western Blot, Polymerase Chain Reaction

    The α7-nAChR/AKT pathway is involved in nicotine-induced SNCG expression. a OEC-M1 cells were pretreated with or without 40 μM PI3K/AKT inhibitor then treated with or without 1 μM nicotine for 24 h. Total proteins were harvested and subjected to Western blot analysis of P-AKT, total AKT, and SNCG expression. GAPDH was also detected as loading control. b OEC-M1 cells with or without α7 nAChR knockdown were plated in cell culture dishes and treated with or without 1 μM nicotine for 24 h. The cell lysates were harvested and subjected to Western blot analysis of P-AKT, total AKT, and SNCG expression

    Journal: Cancer Cell International

    Article Title: Gamma synuclein is a novel nicotine responsive protein in oral cancer malignancy

    doi: 10.1186/s12935-020-01401-w

    Figure Lengend Snippet: The α7-nAChR/AKT pathway is involved in nicotine-induced SNCG expression. a OEC-M1 cells were pretreated with or without 40 μM PI3K/AKT inhibitor then treated with or without 1 μM nicotine for 24 h. Total proteins were harvested and subjected to Western blot analysis of P-AKT, total AKT, and SNCG expression. GAPDH was also detected as loading control. b OEC-M1 cells with or without α7 nAChR knockdown were plated in cell culture dishes and treated with or without 1 μM nicotine for 24 h. The cell lysates were harvested and subjected to Western blot analysis of P-AKT, total AKT, and SNCG expression

    Article Snippet: An anti-GAPDH antibody (Cell Signaling, Danvers, MA, USA), anti-fibronectin antibody (Abcam, Cambridge, England, UK), anti-vimentin antibody (cell signaling), anti-E-cadherin antibody (BD Biosciences, Franklin Lakes, NJ, USA), anti-ZO-1 antibody (BD Biosciences), anti-PCNA antibody (Cell Signaling), anti-protein kinase B (AKT) antibody (Cell Signaling), anti-phospho-AKT (P-AKT) antibody (Cell Signaling), anti-α7-nAChR antibody (Abcam), and anti-SNCG antibody (Cell Signaling) were used for probing.

    Techniques: Expressing, Western Blot, Cell Culture

    α7-nAChR knockdown/inhibition suppresses SNCG expression. a OEC-M1 cells were transfected with plko-1(vector only) or shRNA to α7-nAChR (sh α7-nAChR). Total RNA and proteins were harvested and subjected to RT-PCR and Western blot analysis of α7-nAChR expression. b OEC-M1 OSCC cancer cells were plated in cell culture dishes and treated with or without nicotine for 24 h. The cell lysates were harvested and subjected to RT-PCR and Western blot analysis of SNCG expression. GAPDH was also detected as loading control. c OEC-M1 cells were pretreated with or without MLA, an α7-nAChR inhibitor (MLA), followed by treatment with or without 1 µM nicotine for 24 h. Total RNA and proteins were harvested and subjected to RT-PCR and Western blot analysis of SNCG

    Journal: Cancer Cell International

    Article Title: Gamma synuclein is a novel nicotine responsive protein in oral cancer malignancy

    doi: 10.1186/s12935-020-01401-w

    Figure Lengend Snippet: α7-nAChR knockdown/inhibition suppresses SNCG expression. a OEC-M1 cells were transfected with plko-1(vector only) or shRNA to α7-nAChR (sh α7-nAChR). Total RNA and proteins were harvested and subjected to RT-PCR and Western blot analysis of α7-nAChR expression. b OEC-M1 OSCC cancer cells were plated in cell culture dishes and treated with or without nicotine for 24 h. The cell lysates were harvested and subjected to RT-PCR and Western blot analysis of SNCG expression. GAPDH was also detected as loading control. c OEC-M1 cells were pretreated with or without MLA, an α7-nAChR inhibitor (MLA), followed by treatment with or without 1 µM nicotine for 24 h. Total RNA and proteins were harvested and subjected to RT-PCR and Western blot analysis of SNCG

    Article Snippet: An anti-GAPDH antibody (Cell Signaling, Danvers, MA, USA), anti-fibronectin antibody (Abcam, Cambridge, England, UK), anti-vimentin antibody (cell signaling), anti-E-cadherin antibody (BD Biosciences, Franklin Lakes, NJ, USA), anti-ZO-1 antibody (BD Biosciences), anti-PCNA antibody (Cell Signaling), anti-protein kinase B (AKT) antibody (Cell Signaling), anti-phospho-AKT (P-AKT) antibody (Cell Signaling), anti-α7-nAChR antibody (Abcam), and anti-SNCG antibody (Cell Signaling) were used for probing.

    Techniques: Inhibition, Expressing, Transfection, shRNA, Reverse Transcription Polymerase Chain Reaction, Western Blot, Cell Culture

    α7 nAchR activation induced upregulation of canonical Nrf2 antioxidant genes. a Pretreatment with GTS21 (15 and 30 μm) for 1 h resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, and GCLC, in astrocytes treated with LPS for 24 h. α7 nAchR antagonist MLA (1 μm) significantly reduced this effect indicating the specificity of this response. * p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: α7 nAchR activation induced upregulation of canonical Nrf2 antioxidant genes. a Pretreatment with GTS21 (15 and 30 μm) for 1 h resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, and GCLC, in astrocytes treated with LPS for 24 h. α7 nAchR antagonist MLA (1 μm) significantly reduced this effect indicating the specificity of this response. * p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay

    α7 nAchR activation reduced NF-κB luciferase signal and downregulated pro-inflammatory genes downstream of NF-κB signaling pathway in brain. a Representative images of NF-κB-dependent luminescence in one hemisphere of the brains ( n = 5 mice per group) acquired on the IVIS Spectrum instrument (Perkin Elmer, Hopkinton, MA), using the Perkin Elmer proprietary software, Living Image (v4.3.1). Luciferin was injected intraperitoneally at 150 mg/kg for ex vivo brain imaging, which was conducted after euthanizing the animal and harvesting the brain. b NF-κB-dependent luminescence in the brains of NF-κB luciferase reporter mice was measured by imaging. A significant increase in NF-κB luciferase signal was observed with LPS (1.7 mg/kg) treatment, which was reduced in the presence of GTS21 (25 mg/kg) treatment. * p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: α7 nAchR activation reduced NF-κB luciferase signal and downregulated pro-inflammatory genes downstream of NF-κB signaling pathway in brain. a Representative images of NF-κB-dependent luminescence in one hemisphere of the brains ( n = 5 mice per group) acquired on the IVIS Spectrum instrument (Perkin Elmer, Hopkinton, MA), using the Perkin Elmer proprietary software, Living Image (v4.3.1). Luciferin was injected intraperitoneally at 150 mg/kg for ex vivo brain imaging, which was conducted after euthanizing the animal and harvesting the brain. b NF-κB-dependent luminescence in the brains of NF-κB luciferase reporter mice was measured by imaging. A significant increase in NF-κB luciferase signal was observed with LPS (1.7 mg/kg) treatment, which was reduced in the presence of GTS21 (25 mg/kg) treatment. * p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay, Luciferase, Mouse Assay, Software, Injection, Ex Vivo, Imaging

    Antioxidant and anti-inflammatory responses of α7 nAchR activation are Nrf2 dependent. a Pretreatment with GTS21 (15 and 30 μm) resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, GCLC, and OSGIN1 in wild-type astrocyte cultures treated with LPS (60 ng/ml) for 24 h, but not in astrocytes from Nrf2 knockout mice. * p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: Antioxidant and anti-inflammatory responses of α7 nAchR activation are Nrf2 dependent. a Pretreatment with GTS21 (15 and 30 μm) resulted in significant upregulation of canonical Nrf2 antioxidant genes HO1, TXNRD1, GCLC, and OSGIN1 in wild-type astrocyte cultures treated with LPS (60 ng/ml) for 24 h, but not in astrocytes from Nrf2 knockout mice. * p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay, Knock-Out, Mouse Assay

    α7 nAchR activation reduced inflammatory astrocyte-mediated neuronal apoptosis. a Representative images of caspase activation in neurons treated with astrocyte conditioned media in the presence of LPS (60 ng/ml) for 24 h with or without 1 h GTS21 pretreatment (30 μm). b Quantification of caspase activation upon GTS21 (30 μm) pretreatment for 1 h in LPS (60 ng/ml)-activated astrocyte conditioned media showed significantly lowered levels of caspase 3/7 in neuronal cultures, and this effect was significantly blocked upon addition of 1 μm MLA, * p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: α7 nAchR activation reduced inflammatory astrocyte-mediated neuronal apoptosis. a Representative images of caspase activation in neurons treated with astrocyte conditioned media in the presence of LPS (60 ng/ml) for 24 h with or without 1 h GTS21 pretreatment (30 μm). b Quantification of caspase activation upon GTS21 (30 μm) pretreatment for 1 h in LPS (60 ng/ml)-activated astrocyte conditioned media showed significantly lowered levels of caspase 3/7 in neuronal cultures, and this effect was significantly blocked upon addition of 1 μm MLA, * p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay

    α7 nAchR activation reduced LPS-mediated pro-inflammatory cytokine secretion in astrocytes. a Pretreatment with GTS21 (α7 nAchR agonist) for 1 h resulted in a dose-dependent reduction in both IL-6 and TNF-α secretion as compared to LPS treated alone for 24 h, * p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: α7 nAchR activation reduced LPS-mediated pro-inflammatory cytokine secretion in astrocytes. a Pretreatment with GTS21 (α7 nAchR agonist) for 1 h resulted in a dose-dependent reduction in both IL-6 and TNF-α secretion as compared to LPS treated alone for 24 h, * p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay

    α7 nAchR activation reduced LPS-induced inflammatory genes in astrocytes. a LPS-mediated inflammatory genes were measured using TaqMan® OpenArray® Mouse Inflammation Panel covering 632 inflammatory genes, and changes were plotted on a volcano plot with log fold changes on x -axis and log of corrected p values on y -axis. Red vertical lines indicate boundaries for fold changes. Green dots indicate at least 1.5-fold lower expression and red dots indicate at least 1.5-fold higher expression (both statistically significant at p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: α7 nAchR activation reduced LPS-induced inflammatory genes in astrocytes. a LPS-mediated inflammatory genes were measured using TaqMan® OpenArray® Mouse Inflammation Panel covering 632 inflammatory genes, and changes were plotted on a volcano plot with log fold changes on x -axis and log of corrected p values on y -axis. Red vertical lines indicate boundaries for fold changes. Green dots indicate at least 1.5-fold lower expression and red dots indicate at least 1.5-fold higher expression (both statistically significant at p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay, Expressing

    α7 nAchR activation resulted in inhibition of the NF-κB signaling pathway and astrogliosis. a Pretreatment with GTS21 (15 and 30 μm) resulted in reduction of phosphorylated form of IκBα in LPS (60 ng/ml)-treated astrocytes for 30 min. b Treatment of astrocytes with LPS (60 ng/ml) for 3 h caused robust nuclear translocation of NF-κB and pretreatment with α7 nAchR agonist GTS21 (30 μm) for 1 h caused significant reduction in NF-κB nuclear translocation, * p

    Journal: Journal of Neuroinflammation

    Article Title: Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

    doi: 10.1186/s12974-017-0967-6

    Figure Lengend Snippet: α7 nAchR activation resulted in inhibition of the NF-κB signaling pathway and astrogliosis. a Pretreatment with GTS21 (15 and 30 μm) resulted in reduction of phosphorylated form of IκBα in LPS (60 ng/ml)-treated astrocytes for 30 min. b Treatment of astrocytes with LPS (60 ng/ml) for 3 h caused robust nuclear translocation of NF-κB and pretreatment with α7 nAchR agonist GTS21 (30 μm) for 1 h caused significant reduction in NF-κB nuclear translocation, * p

    Article Snippet: α7 nAchRs are expressed in mouse astrocytes To evaluate the expression of α7 nAChRs in primary astrocyte cultures, we performed quantitative RT-PCR using TaqMan probes specific for α7 nAChR (Applied Biosystem (ThermoFisher Scientific) assay ID Mm01312230_m1).

    Techniques: Activation Assay, Inhibition, Translocation Assay

    α7 nAchR negatively regulates inflammasome activation. (A) LPS-primed peritoneal mouse macrophages from either WT or α7 nAchR knockout (a7 KO) mice were stimulated with ATP in the presence or the absence of acetylcholine for 30 min. (B)

    Journal: Molecular Medicine

    Article Title: α7 Nicotinic Acetylcholine Receptor Signaling Inhibits Inflammasome Activation by Preventing Mitochondrial DNA Release

    doi: 10.2119/molmed.2013.00117

    Figure Lengend Snippet: α7 nAchR negatively regulates inflammasome activation. (A) LPS-primed peritoneal mouse macrophages from either WT or α7 nAchR knockout (a7 KO) mice were stimulated with ATP in the presence or the absence of acetylcholine for 30 min. (B)

    Article Snippet: Plasmids expressing procaspase-1, ASC, NLRP3 or α7 nAchR were purchased from Origene (Rockville, MD, USA).

    Techniques: Activation Assay, Knock-Out, Mouse Assay

    Codistribution of tSNAREs with α7-nAChR clusters on CG neurons. Freshly dissociated E14 CG neurons were costained with AlexaαBgt for α7-nAChRs ( A, D, G, J ) and antibodies for SNAP-25 ( B ), syntaxin 1 ( E ), SV2 ( H ), or nonimmune serum as a negative control ( K ), and the corresponding pairs of fluorescence images were merged ( C, F, I, L ). Both SNAP-25 and syntaxin 1 codistribute with α7-nAChRs. Similar results were obtained in three additional experiments. Scale bar, 10 μm.

    Journal: The Journal of Neuroscience

    Article Title: Rapid Activity-Driven SNARE-Dependent Trafficking of Nicotinic Receptors on Somatic Spines

    doi: 10.1523/JNEUROSCI.3953-04.2005

    Figure Lengend Snippet: Codistribution of tSNAREs with α7-nAChR clusters on CG neurons. Freshly dissociated E14 CG neurons were costained with AlexaαBgt for α7-nAChRs ( A, D, G, J ) and antibodies for SNAP-25 ( B ), syntaxin 1 ( E ), SV2 ( H ), or nonimmune serum as a negative control ( K ), and the corresponding pairs of fluorescence images were merged ( C, F, I, L ). Both SNAP-25 and syntaxin 1 codistribute with α7-nAChRs. Similar results were obtained in three additional experiments. Scale bar, 10 μm.

    Article Snippet: Thresholds of 10 and 15% of maximum were chosen for α7-nAChR and syntaxin 1 clusters, respectively, in colabeling experiments; thresholds of 16 and 24% of maximum were chosen for α7-nAChR and FM4-64 puncta, respectively, in dye-uptake experiments.

    Techniques: Negative Control, Fluorescence

    Synthesis of α7 nAChR ligands. Reagents and conditions: (a) ArCOCH 2- CO 2 Me, i-BuOH, 100 °C, overnight; (b) methyl 2-(cyanomethoxy)benzoate, CS 2 (one drop), 100–110 °C, overnight; (c) (2-cyanophenoxy)acetonitrile, CS 2 (one

    Journal: European journal of medicinal chemistry

    Article Title: Docking studies of benzylidene anabaseine interactions with α7 nicotinic acetylcholine receptor (nAChR) and acetylcholine binding proteins (AChBPs): Application to the design of related α7 selective ligands

    doi: 10.1016/j.ejmech.2011.09.033

    Figure Lengend Snippet: Synthesis of α7 nAChR ligands. Reagents and conditions: (a) ArCOCH 2- CO 2 Me, i-BuOH, 100 °C, overnight; (b) methyl 2-(cyanomethoxy)benzoate, CS 2 (one drop), 100–110 °C, overnight; (c) (2-cyanophenoxy)acetonitrile, CS 2 (one

    Article Snippet: Chantix® , a partial agonist at α4β2 and a full agonist at α7 nAChR from Pfizer, has recently been launched for smoking cessation [ , ].

    Techniques:

    GABAergic synapse formation was impaired in the prefrontal cortex of α7 nAChR null mice during late postnatal development and adulthood

    Journal: Molecular and cellular neurosciences

    Article Title: Cortical parvalbumin GABAergic deficits with α7 nicotinic acetylcholine receptor deletion: Implications for schizophrenia

    doi: 10.1016/j.mcn.2014.06.007

    Figure Lengend Snippet: GABAergic synapse formation was impaired in the prefrontal cortex of α7 nAChR null mice during late postnatal development and adulthood

    Article Snippet: Timed-pregnant C57BL/6 mice were purchased from Charles River Laboratories and bred from α7 nAChR knockout mice (B6.129S7-Chrna7tm1Bay /J, Jackson Laboratory).

    Techniques: Mouse Assay

    The levels of PV, GAD65/67 and GABA A α1 were decreased in the prefrontal cortex of α7 nAChR null mice during late postnatal development and adulthood

    Journal: Molecular and cellular neurosciences

    Article Title: Cortical parvalbumin GABAergic deficits with α7 nicotinic acetylcholine receptor deletion: Implications for schizophrenia

    doi: 10.1016/j.mcn.2014.06.007

    Figure Lengend Snippet: The levels of PV, GAD65/67 and GABA A α1 were decreased in the prefrontal cortex of α7 nAChR null mice during late postnatal development and adulthood

    Article Snippet: Timed-pregnant C57BL/6 mice were purchased from Charles River Laboratories and bred from α7 nAChR knockout mice (B6.129S7-Chrna7tm1Bay /J, Jackson Laboratory).

    Techniques: Mouse Assay

    The levels of PV, but not somatostatin, immunoreactivities were decreased in the prefrontal cortex of α7 nAChR null mice during late postnatal development and adulthood

    Journal: Molecular and cellular neurosciences

    Article Title: Cortical parvalbumin GABAergic deficits with α7 nicotinic acetylcholine receptor deletion: Implications for schizophrenia

    doi: 10.1016/j.mcn.2014.06.007

    Figure Lengend Snippet: The levels of PV, but not somatostatin, immunoreactivities were decreased in the prefrontal cortex of α7 nAChR null mice during late postnatal development and adulthood

    Article Snippet: Timed-pregnant C57BL/6 mice were purchased from Charles River Laboratories and bred from α7 nAChR knockout mice (B6.129S7-Chrna7tm1Bay /J, Jackson Laboratory).

    Techniques: Mouse Assay

    PV and GAD67 levels in PV-positive GABAergic interneurons as well as GABA A α1 levels in pyramidal neurons were reduced in mouse prefrontal cortex with α7 nAChR deletion during late postnatal development and adulthood

    Journal: Molecular and cellular neurosciences

    Article Title: Cortical parvalbumin GABAergic deficits with α7 nicotinic acetylcholine receptor deletion: Implications for schizophrenia

    doi: 10.1016/j.mcn.2014.06.007

    Figure Lengend Snippet: PV and GAD67 levels in PV-positive GABAergic interneurons as well as GABA A α1 levels in pyramidal neurons were reduced in mouse prefrontal cortex with α7 nAChR deletion during late postnatal development and adulthood

    Article Snippet: Timed-pregnant C57BL/6 mice were purchased from Charles River Laboratories and bred from α7 nAChR knockout mice (B6.129S7-Chrna7tm1Bay /J, Jackson Laboratory).

    Techniques:

    Cortical levels of GABAergic markers were decreased in α7 nAChR null mice during late postnatal development and adulthood

    Journal: Molecular and cellular neurosciences

    Article Title: Cortical parvalbumin GABAergic deficits with α7 nicotinic acetylcholine receptor deletion: Implications for schizophrenia

    doi: 10.1016/j.mcn.2014.06.007

    Figure Lengend Snippet: Cortical levels of GABAergic markers were decreased in α7 nAChR null mice during late postnatal development and adulthood

    Article Snippet: Timed-pregnant C57BL/6 mice were purchased from Charles River Laboratories and bred from α7 nAChR knockout mice (B6.129S7-Chrna7tm1Bay /J, Jackson Laboratory).

    Techniques: Mouse Assay

    Effects of EA on the expression of α7-nAChR (A) Immunofluorescence analysis was performed to determine α7-nAChR expression on Tiabilis anterior muscle 14 days after the procedure. The samples were immunostained with an anti-α7-nAChR-antibody (red, → marks a positive expression). The result shows that α7-nAChR expression are sharply increased and clustered on the muscle membrane of rats in the immobilization group. Representative results from three independent experiments are shown here (scale bar = 50 μm). (B) The Western blot analysis of the α7-nAChR proteins are shown for each groups. Relative intensity of α7-nAChR to GAPDH is shown in the graphs. α7-nAChR significantly increased after the immobilization for 14 days. Electroacupuncture suppressed the expression of α7-nAChR in EA group. All values are expressed as means ± SD (n=6/group). # P

    Journal: Oncotarget

    Article Title: Electroacupuncture alleviates neuromuscular dysfunction in an experimental rat model of immobilization

    doi: 10.18632/oncotarget.20246

    Figure Lengend Snippet: Effects of EA on the expression of α7-nAChR (A) Immunofluorescence analysis was performed to determine α7-nAChR expression on Tiabilis anterior muscle 14 days after the procedure. The samples were immunostained with an anti-α7-nAChR-antibody (red, → marks a positive expression). The result shows that α7-nAChR expression are sharply increased and clustered on the muscle membrane of rats in the immobilization group. Representative results from three independent experiments are shown here (scale bar = 50 μm). (B) The Western blot analysis of the α7-nAChR proteins are shown for each groups. Relative intensity of α7-nAChR to GAPDH is shown in the graphs. α7-nAChR significantly increased after the immobilization for 14 days. Electroacupuncture suppressed the expression of α7-nAChR in EA group. All values are expressed as means ± SD (n=6/group). # P

    Article Snippet: After washing in phosphate-buffered saline, these sections were incubated with fluorescein isothiocyanate-conjugated Goat anti-rabbit IgG antibody to stain for α7-nAChR (dilution 1:200; #A23320 Abbkine, Inc, California, USA) or Goat anti-rabbit IgG antibody for γ-nAChR (dilution 1:200; #A23220 Abbkine, Inc, California, USA) for 1h at room temperature to detect each primary antibody.

    Techniques: Expressing, Immunofluorescence, Western Blot