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nsc34 neurons  (Cedarlane)


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    Cedarlane nsc34 neurons
    PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated <t>NSC34</t> neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
    Nsc34 Neurons, supplied by Cedarlane, used in various techniques. Bioz Stars score: 93/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Development of a PTEN -siRNA activated scaffold to promote axonal regrowth following spinal cord injury"

    Article Title: Development of a PTEN -siRNA activated scaffold to promote axonal regrowth following spinal cord injury

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.01.022

    PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated NSC34 neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
    Figure Legend Snippet: PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated NSC34 neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

    Techniques Used: Transfection, Knockdown, One-tailed Test, Expressing, Activity Assay, Control, Staining

    Scaffold-mediated siRNA delivery does not affect the viability of neurons, results in prolonged downregulation of PTEN, and stimulates increased expression of BCL2 and GAP43 mRNA . (A) The metabolic activity of NSC34 neurons cultured on PTEN -siRNA activated scaffolds peaked by day 3 post-transfection [t(2) = 4.0599, p = 0.05565, 95 % CI 93.954<x<308.3], decreased by day 7 [t(2) = −15.068, p = 0.004375, 95 % CI 49.7157<x<72.05] and was similar to control levels by day 21 [t(2) = −0.1042, p = 0.9265, 95 % CI 83.23<x<116.0]. Metabolic activity normalization was performed relative to the untreated cells. (B) LDH assay revealed a consistent but small increase in cell stress over a span of 21 days. (C – D) Analysis of PTEN gene expression in scaffold transfected neurons over 21 days showed a significant decrease in expression levels [t(4) = −3.2927, p = 0.01507; one-tailed] 3 days after transfection that was then followed by a gradual return toward untreated control levels denoted by the blue regression line which approaches the red untreated control line after 21 days. (E – F) The change in BCL2 expression 3-, 7-, and 21-days post-transfection showed a significant initial elevation [t(4) = 2.092, p = 0.05227, one-tailed], followed by a gradual reduction converging toward untreated control levels. (G – H). Similarly, GAP43 expression was characterised by of an initial significant rise [t(4) = 2.1748, p = 0.04765, one-tailed] in levels that was followed by a decrease over the 21-day culture period. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.
    Figure Legend Snippet: Scaffold-mediated siRNA delivery does not affect the viability of neurons, results in prolonged downregulation of PTEN, and stimulates increased expression of BCL2 and GAP43 mRNA . (A) The metabolic activity of NSC34 neurons cultured on PTEN -siRNA activated scaffolds peaked by day 3 post-transfection [t(2) = 4.0599, p = 0.05565, 95 % CI 93.954 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

    Techniques Used: Expressing, Activity Assay, Cell Culture, Transfection, Control, Lactate Dehydrogenase Assay, Gene Expression, One-tailed Test



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    Effect of APG on viability and apoptosis in <t>NSC34</t> neuronal cells. A CCK8 assay to evaluate the effects of different doses of APG on the viability of NSC34 cells in vitro. B Flow cytometry analysis of apoptosis in NSC34 cells harboring the SOD1*G93A mutation treated with APG. C Western blot analysis of apoptosis-related proteins (Bcl-2, caspase-3, Bax) in SOD1*G93A mutant NSC34 cells treated with APG. D Flow cytometry assessment of ROS levels in SOD1*G93A mutant NSC34 cells under APG treatment. E - H ELISA for quantification of OS markers (MDA, 4-HNE, SOD, ALDH) in SOD1*G93A mutant NSC34 cells treated with APG. I qRT-PCR analysis of ALDH1A2 mRNA levels, and (J) Western blot analysis of ALDH1A2 protein levels in APG-treated SOD1*G93A mutant NSC34 cells. * P < 0.05, ** P < 0.01, * P < 0.001
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    Fig. 3. Overexpression of RBM5 induces motor neurons apoptosis. (A) Western blotting analysis and qRT-PCR were performed to assess the efficiency of RBM5 overexpression (n=3). (B) Flow cytometry was employed to assess the apoptosis of <t>NSC34</t> cells following transfection with RBM5 or EV plasmid for 48 h (n=3). (C) TUNEL staining of NSC34 cells after treatment with RBM5 or EV plasmid (n=3). (D) Cell viability was quantified using CCK-8 (n=5). Data are presented as means ± SD. Statistical analysis was performed using student’s t-test. *p<0.05, **p<0.01, ***p<0.001.
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    Fig. 3. Overexpression of RBM5 induces motor neurons apoptosis. (A) Western blotting analysis and qRT-PCR were performed to assess the efficiency of RBM5 overexpression (n=3). (B) Flow cytometry was employed to assess the apoptosis of <t>NSC34</t> cells following transfection with RBM5 or EV plasmid for 48 h (n=3). (C) TUNEL staining of NSC34 cells after treatment with RBM5 or EV plasmid (n=3). (D) Cell viability was quantified using CCK-8 (n=5). Data are presented as means ± SD. Statistical analysis was performed using student’s t-test. *p<0.05, **p<0.01, ***p<0.001.
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    Image Search Results


    PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated NSC34 neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820<x <134.3874] and 7 days [t(2) = −3.390, p = 0.07708, 95 % CI -66.21<x<104.0] post-transfection. (C – F) Transfection of PTEN -siRNA nanoparticles does not affect neuronal morphology. Control and PTEN -siRNA nanoparticle treated neurons have a similar distribution, density, and morphology compared to control neurons (C, D). Higher magnification images showed that all neurons (control and treated) possessed a typical neuronal morphology with several neurites extending from each cell body (E, F). All cells were stained for F-actin (green = phalloidin) and nuclei (blue = DAPI). Scale Bar in (C, D): 100 μm; Scale Bar in (E, F): 50 μm. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

    Journal: Bioactive Materials

    Article Title: Development of a PTEN -siRNA activated scaffold to promote axonal regrowth following spinal cord injury

    doi: 10.1016/j.bioactmat.2026.01.022

    Figure Lengend Snippet: PTEN -siRNA nanoparticle transfection enables efficient gene silencing with minimal impact on neuron health (A) PTEN -siRNA nanoparticles (100 nM) demonstrated highly efficient knockdown of target PTEN mRNA in differentiated NSC34 neurons, with peak knockdown on Day 3 for the delivered siRNA [t(2) = −4.840, p = 0.02007; one-tailed] with expression levels returning to baseline by Day 7 [t(2) = 0.05373, p = 0.5190; one-tailed]. RNA fold change and associated error was assessed using the 2 −ΔΔCt method and normalized to GAPDH as per (B) Treatment of neurons with PTEN- siRNA nanoparticles at 100 nM had a non-significant effect on the metabolic activity at 3 [t(2) = 0.6370, p = 0.5893, 95 % CI 74.4820 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

    Article Snippet: NSC34 neuronal culture and transfections: NSC34 neurons (Cedarlane Cat No. CLU140), a hybrid cell line produced by the fusion of motor neuron enriched embryonic mouse spinal cord cells with mouse neuroblastoma cells, were cultured in growth medium Dulbecco's Modified Eagle Medium (DMEM; Sigma-Aldrich, Ireland) supplemented with 10 % fetal bovine serum (FBS; Labtech UK), 1 % (v/v) L-Glutamine (Sigma-Aldrich, Ireland), and 1 % (v/v) Penicillin- Streptomycin Solution (Sigma-Aldrich, Ireland) in a T-175 cell culture flask (37 °C, 5 % CO 2 ).

    Techniques: Transfection, Knockdown, One-tailed Test, Expressing, Activity Assay, Control, Staining

    Scaffold-mediated siRNA delivery does not affect the viability of neurons, results in prolonged downregulation of PTEN, and stimulates increased expression of BCL2 and GAP43 mRNA . (A) The metabolic activity of NSC34 neurons cultured on PTEN -siRNA activated scaffolds peaked by day 3 post-transfection [t(2) = 4.0599, p = 0.05565, 95 % CI 93.954<x<308.3], decreased by day 7 [t(2) = −15.068, p = 0.004375, 95 % CI 49.7157<x<72.05] and was similar to control levels by day 21 [t(2) = −0.1042, p = 0.9265, 95 % CI 83.23<x<116.0]. Metabolic activity normalization was performed relative to the untreated cells. (B) LDH assay revealed a consistent but small increase in cell stress over a span of 21 days. (C – D) Analysis of PTEN gene expression in scaffold transfected neurons over 21 days showed a significant decrease in expression levels [t(4) = −3.2927, p = 0.01507; one-tailed] 3 days after transfection that was then followed by a gradual return toward untreated control levels denoted by the blue regression line which approaches the red untreated control line after 21 days. (E – F) The change in BCL2 expression 3-, 7-, and 21-days post-transfection showed a significant initial elevation [t(4) = 2.092, p = 0.05227, one-tailed], followed by a gradual reduction converging toward untreated control levels. (G – H). Similarly, GAP43 expression was characterised by of an initial significant rise [t(4) = 2.1748, p = 0.04765, one-tailed] in levels that was followed by a decrease over the 21-day culture period. Significance code: ns = p > 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

    Journal: Bioactive Materials

    Article Title: Development of a PTEN -siRNA activated scaffold to promote axonal regrowth following spinal cord injury

    doi: 10.1016/j.bioactmat.2026.01.022

    Figure Lengend Snippet: Scaffold-mediated siRNA delivery does not affect the viability of neurons, results in prolonged downregulation of PTEN, and stimulates increased expression of BCL2 and GAP43 mRNA . (A) The metabolic activity of NSC34 neurons cultured on PTEN -siRNA activated scaffolds peaked by day 3 post-transfection [t(2) = 4.0599, p = 0.05565, 95 % CI 93.954 0.1; • = p ≤ 0.1, ∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001, ∗∗∗∗ = p ≤ 0.0001.

    Article Snippet: NSC34 neuronal culture and transfections: NSC34 neurons (Cedarlane Cat No. CLU140), a hybrid cell line produced by the fusion of motor neuron enriched embryonic mouse spinal cord cells with mouse neuroblastoma cells, were cultured in growth medium Dulbecco's Modified Eagle Medium (DMEM; Sigma-Aldrich, Ireland) supplemented with 10 % fetal bovine serum (FBS; Labtech UK), 1 % (v/v) L-Glutamine (Sigma-Aldrich, Ireland), and 1 % (v/v) Penicillin- Streptomycin Solution (Sigma-Aldrich, Ireland) in a T-175 cell culture flask (37 °C, 5 % CO 2 ).

    Techniques: Expressing, Activity Assay, Cell Culture, Transfection, Control, Lactate Dehydrogenase Assay, Gene Expression, One-tailed Test

    Effect of APG on viability and apoptosis in NSC34 neuronal cells. A CCK8 assay to evaluate the effects of different doses of APG on the viability of NSC34 cells in vitro. B Flow cytometry analysis of apoptosis in NSC34 cells harboring the SOD1*G93A mutation treated with APG. C Western blot analysis of apoptosis-related proteins (Bcl-2, caspase-3, Bax) in SOD1*G93A mutant NSC34 cells treated with APG. D Flow cytometry assessment of ROS levels in SOD1*G93A mutant NSC34 cells under APG treatment. E - H ELISA for quantification of OS markers (MDA, 4-HNE, SOD, ALDH) in SOD1*G93A mutant NSC34 cells treated with APG. I qRT-PCR analysis of ALDH1A2 mRNA levels, and (J) Western blot analysis of ALDH1A2 protein levels in APG-treated SOD1*G93A mutant NSC34 cells. * P < 0.05, ** P < 0.01, * P < 0.001

    Journal: Molecular Medicine

    Article Title: The therapeutic potential of Apigenin in amyotrophic lateral sclerosis through ALDH1A2/Nrf2/ARE signaling

    doi: 10.1186/s10020-024-00977-7

    Figure Lengend Snippet: Effect of APG on viability and apoptosis in NSC34 neuronal cells. A CCK8 assay to evaluate the effects of different doses of APG on the viability of NSC34 cells in vitro. B Flow cytometry analysis of apoptosis in NSC34 cells harboring the SOD1*G93A mutation treated with APG. C Western blot analysis of apoptosis-related proteins (Bcl-2, caspase-3, Bax) in SOD1*G93A mutant NSC34 cells treated with APG. D Flow cytometry assessment of ROS levels in SOD1*G93A mutant NSC34 cells under APG treatment. E - H ELISA for quantification of OS markers (MDA, 4-HNE, SOD, ALDH) in SOD1*G93A mutant NSC34 cells treated with APG. I qRT-PCR analysis of ALDH1A2 mRNA levels, and (J) Western blot analysis of ALDH1A2 protein levels in APG-treated SOD1*G93A mutant NSC34 cells. * P < 0.05, ** P < 0.01, * P < 0.001

    Article Snippet: 293FT and NSC34 cell lines from Procell (Wuhan, China) were cultured in DMEM containing 10% fetal bovine serum (FBS) at 37 °C.

    Techniques: CCK-8 Assay, In Vitro, Flow Cytometry, Mutagenesis, Western Blot, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    Effects of ALDH1A2 knockdown and APG treatment on ALS model and OS markers. A - B Validation and selection of the most effective sh-ALDH1A2 to suppress ALDH1A2 expression by qRT-PCR and Western blot analysis. C Flow cytometry to evaluate apoptosis in NSC34 cells treated with APG and sh-ALDH1A2. D Western blot to evaluate the levels of apoptosis-related proteins (Bcl-2, caspase-3, Bax) in NSC34 cells treated with both APG and sh-ALDH1A2. E Flow cytometric analysis of ROS levels in treated NSC34 cells. F - I ELISA for quantification of OS markers (MDA, 4-HNE, SOD, ALDH) in NSC34 cells treated with APG and sh-ALDH1A2. J Western blot analysis of ALDH1A2 protein levels. K - L qRT-PCR and Western blot analysis of Nrf2, HO-1, NQO1 mRNA and protein levels in NSC34 cells treated with APG and sh-ALDH1A2. * P < 0.05, ** P < 0.01, * P < 0.001

    Journal: Molecular Medicine

    Article Title: The therapeutic potential of Apigenin in amyotrophic lateral sclerosis through ALDH1A2/Nrf2/ARE signaling

    doi: 10.1186/s10020-024-00977-7

    Figure Lengend Snippet: Effects of ALDH1A2 knockdown and APG treatment on ALS model and OS markers. A - B Validation and selection of the most effective sh-ALDH1A2 to suppress ALDH1A2 expression by qRT-PCR and Western blot analysis. C Flow cytometry to evaluate apoptosis in NSC34 cells treated with APG and sh-ALDH1A2. D Western blot to evaluate the levels of apoptosis-related proteins (Bcl-2, caspase-3, Bax) in NSC34 cells treated with both APG and sh-ALDH1A2. E Flow cytometric analysis of ROS levels in treated NSC34 cells. F - I ELISA for quantification of OS markers (MDA, 4-HNE, SOD, ALDH) in NSC34 cells treated with APG and sh-ALDH1A2. J Western blot analysis of ALDH1A2 protein levels. K - L qRT-PCR and Western blot analysis of Nrf2, HO-1, NQO1 mRNA and protein levels in NSC34 cells treated with APG and sh-ALDH1A2. * P < 0.05, ** P < 0.01, * P < 0.001

    Article Snippet: 293FT and NSC34 cell lines from Procell (Wuhan, China) were cultured in DMEM containing 10% fetal bovine serum (FBS) at 37 °C.

    Techniques: Knockdown, Biomarker Discovery, Selection, Expressing, Quantitative RT-PCR, Western Blot, Flow Cytometry, Enzyme-linked Immunosorbent Assay

    Fig. 3. Overexpression of RBM5 induces motor neurons apoptosis. (A) Western blotting analysis and qRT-PCR were performed to assess the efficiency of RBM5 overexpression (n=3). (B) Flow cytometry was employed to assess the apoptosis of NSC34 cells following transfection with RBM5 or EV plasmid for 48 h (n=3). (C) TUNEL staining of NSC34 cells after treatment with RBM5 or EV plasmid (n=3). (D) Cell viability was quantified using CCK-8 (n=5). Data are presented as means ± SD. Statistical analysis was performed using student’s t-test. *p<0.05, **p<0.01, ***p<0.001.

    Journal: Brain research bulletin

    Article Title: RBM5 induces motor neuron apoptosis in hSOD1 G93A -related amyotrophic lateral sclerosis by inhibiting Rac1/AKT pathways.

    doi: 10.1016/j.brainresbull.2024.111049

    Figure Lengend Snippet: Fig. 3. Overexpression of RBM5 induces motor neurons apoptosis. (A) Western blotting analysis and qRT-PCR were performed to assess the efficiency of RBM5 overexpression (n=3). (B) Flow cytometry was employed to assess the apoptosis of NSC34 cells following transfection with RBM5 or EV plasmid for 48 h (n=3). (C) TUNEL staining of NSC34 cells after treatment with RBM5 or EV plasmid (n=3). (D) Cell viability was quantified using CCK-8 (n=5). Data are presented as means ± SD. Statistical analysis was performed using student’s t-test. *p<0.05, **p<0.01, ***p<0.001.

    Article Snippet: The NSC34 cell line (Cedarlane Laboratories, Vancouver, Canada) is a hybrid of embryonic mouse neuroblastoma and spinal cord motor neurons.

    Techniques: Over Expression, Western Blot, Quantitative RT-PCR, Flow Cytometry, Transfection, Plasmid Preparation, TUNEL Assay, Staining, CCK-8 Assay