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lps col4a2 wt group  (MedChemExpress)


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    MedChemExpress lps col4a2 wt group
    Summary of the genetic findings of our 8 patients
    Lps Col4a2 Wt Group, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 680 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/lps+col4a2+wt+group/Lipopolysaccharides/pmc11241092-109-37-89
    Average 99 stars, based on 680 article reviews
    lps col4a2 wt group - by Bioz Stars, 2026-09
    99/100 stars

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    1) Product Images from "Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation"

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation

    Journal: International Journal of Medical Sciences

    doi: 10.7150/ijms.97164

    Summary of the genetic findings of our 8 patients
    Figure Legend Snippet: Summary of the genetic findings of our 8 patients

    Techniques Used:

    Mutation of Col4a2 promotes inflammation and astrocyte activation in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different groups, with 50 CTX-TNA cells per group from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to quantify IL-1β, IL-6, and TNF-α levels in the supernatant of CTX-TNA cells from 3 repeated experiments. The figure includes results from one-way ANOVA with calculated p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.
    Figure Legend Snippet: Mutation of Col4a2 promotes inflammation and astrocyte activation in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different groups, with 50 CTX-TNA cells per group from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to quantify IL-1β, IL-6, and TNF-α levels in the supernatant of CTX-TNA cells from 3 repeated experiments. The figure includes results from one-way ANOVA with calculated p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.

    Techniques Used: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot

    Col4a2 mutation promotes inflammation and astrocyte activation in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with either the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different primary astrocyte groups, with 50 cells per group from 3 repeated experiments. The scale bar indicates 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to measure IL-1β, IL-6, and TNF-α levels in primary astrocyte supernatants from 3 repeated experiments. The figure includes one-way ANOVA results with corresponding p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.
    Figure Legend Snippet: Col4a2 mutation promotes inflammation and astrocyte activation in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with either the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different primary astrocyte groups, with 50 cells per group from 3 repeated experiments. The scale bar indicates 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to measure IL-1β, IL-6, and TNF-α levels in primary astrocyte supernatants from 3 repeated experiments. The figure includes one-way ANOVA results with corresponding p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.

    Techniques Used: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot, Control

    Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP was observed in 6 different groups (50 CTX-TNA cells per group) from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). The figure includes the results of one-way ANOVA with calculated p values. (C) Western blot analysis of GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3 was performed. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.
    Figure Legend Snippet: Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP was observed in 6 different groups (50 CTX-TNA cells per group) from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). The figure includes the results of one-way ANOVA with calculated p values. (C) Western blot analysis of GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3 was performed. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.

    Techniques Used: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot

    Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP in six different primary astrocyte groups (50 cells per group) from 3 repeated experiments is shown. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). One-way ANOVA with calculated p values is presented in the figure. (C) Western blot analysis was conducted for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.
    Figure Legend Snippet: Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP in six different primary astrocyte groups (50 cells per group) from 3 repeated experiments is shown. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). One-way ANOVA with calculated p values is presented in the figure. (C) Western blot analysis was conducted for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.

    Techniques Used: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot, Control

    Related Articles

    Control:

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation
    Article Snippet: The cells were cultured in DMEM (Gibco, USA) supplemented with 10% FBS (Gibco, USA) and 1% penicillin‒streptomycin (SolarBio, China) at 37 °C with 5% CO 2 . .. The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector). ..

    Transfection:

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation
    Article Snippet: The cells were cultured in DMEM (Gibco, USA) supplemented with 10% FBS (Gibco, USA) and 1% penicillin‒streptomycin (SolarBio, China) at 37 °C with 5% CO 2 . .. The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector). ..

    Mutagenesis:

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation
    Article Snippet: The cells were cultured in DMEM (Gibco, USA) supplemented with 10% FBS (Gibco, USA) and 1% penicillin‒streptomycin (SolarBio, China) at 37 °C with 5% CO 2 . .. The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector). ..

    Plasmid Preparation:

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation
    Article Snippet: The cells were cultured in DMEM (Gibco, USA) supplemented with 10% FBS (Gibco, USA) and 1% penicillin‒streptomycin (SolarBio, China) at 37 °C with 5% CO 2 . .. The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector). ..



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    lps col4a2 wt group  (MedChemExpress)
    99
    MedChemExpress lps col4a2 wt group
    Summary of the genetic findings of our 8 patients
    Lps Col4a2 Wt Group, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/lps+col4a2+wt+group/Lipopolysaccharides/pmc11241092-109-37-89
    Average 99 stars, based on 1 article reviews
    lps col4a2 wt group - by Bioz Stars, 2026-09
    99/100 stars
    		  Buy from Supplier

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    Summary of the genetic findings of our 8 patients

    Journal: International Journal of Medical Sciences

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation

    doi: 10.7150/ijms.97164

    Figure Lengend Snippet: Summary of the genetic findings of our 8 patients

    Article Snippet: The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector).

    Techniques:

    Mutation of Col4a2 promotes inflammation and astrocyte activation in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different groups, with 50 CTX-TNA cells per group from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to quantify IL-1β, IL-6, and TNF-α levels in the supernatant of CTX-TNA cells from 3 repeated experiments. The figure includes results from one-way ANOVA with calculated p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.

    Journal: International Journal of Medical Sciences

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation

    doi: 10.7150/ijms.97164

    Figure Lengend Snippet: Mutation of Col4a2 promotes inflammation and astrocyte activation in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different groups, with 50 CTX-TNA cells per group from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to quantify IL-1β, IL-6, and TNF-α levels in the supernatant of CTX-TNA cells from 3 repeated experiments. The figure includes results from one-way ANOVA with calculated p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.

    Article Snippet: The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector).

    Techniques: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot

    Col4a2 mutation promotes inflammation and astrocyte activation in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with either the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different primary astrocyte groups, with 50 cells per group from 3 repeated experiments. The scale bar indicates 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to measure IL-1β, IL-6, and TNF-α levels in primary astrocyte supernatants from 3 repeated experiments. The figure includes one-way ANOVA results with corresponding p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.

    Journal: International Journal of Medical Sciences

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation

    doi: 10.7150/ijms.97164

    Figure Lengend Snippet: Col4a2 mutation promotes inflammation and astrocyte activation in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with either the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector. (A) The fluorescence intensity of GFAP (red) was measured in 5 different primary astrocyte groups, with 50 cells per group from 3 repeated experiments. The scale bar indicates 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). (C-E) Enzyme-linked immunosorbent assays were used to measure IL-1β, IL-6, and TNF-α levels in primary astrocyte supernatants from 3 repeated experiments. The figure includes one-way ANOVA results with corresponding p values. (F) Western blot analysis was performed for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01.

    Article Snippet: The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector).

    Techniques: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot, Control

    Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP was observed in 6 different groups (50 CTX-TNA cells per group) from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). The figure includes the results of one-way ANOVA with calculated p values. (C) Western blot analysis of GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3 was performed. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.

    Journal: International Journal of Medical Sciences

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation

    doi: 10.7150/ijms.97164

    Figure Lengend Snippet: Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in CTX-TNA cells. CTX-TNA cells were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP was observed in 6 different groups (50 CTX-TNA cells per group) from 3 repeated experiments. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). The figure includes the results of one-way ANOVA with calculated p values. (C) Western blot analysis of GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3 was performed. The proteins for the western blot analysis were extracted from cell lysates. **: vs. con, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.

    Article Snippet: The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector).

    Techniques: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot

    Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP in six different primary astrocyte groups (50 cells per group) from 3 repeated experiments is shown. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). One-way ANOVA with calculated p values is presented in the figure. (C) Western blot analysis was conducted for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.

    Journal: International Journal of Medical Sciences

    Article Title: Col4a2 Mutations Contribute to Infantile Epileptic Spasm Syndrome and Neuroinflammation

    doi: 10.7150/ijms.97164

    Figure Lengend Snippet: Col4a2 mutation promotes inflammation and astrocyte activation by stimulating JAK/STAT signaling in primary astrocytes. Primary astrocytes were stimulated with LPS and transfected with the Col4a2 Wt -AdV vector or the Col4a2 Mut -AdV vector or treated with WP1066 (a JAK2/STAT inhibitor). (A) The fluorescence intensity of GFAP in six different primary astrocyte groups (50 cells per group) from 3 repeated experiments is shown. The scale bar represents 25 μm. (B) Quantitative graphs displaying the mean fluorescence intensity of the GFAP-positive cells in (A). One-way ANOVA with calculated p values is presented in the figure. (C) Western blot analysis was conducted for GFAP, IL-1β, IL-6, TNF-α, JAK2, p-JAK2, STAT3, and p-STAT3. The proteins for the western blot analysis were extracted from cell lysates. **: vs. control, p<0.01; ++: vs. LPS+NC, p<0.01; ##: vs. LPS+ Col4a2 Wt , p <0.01; ^^: vs. LPS+ Col4a2 Mut , p<0.01.

    Article Snippet: The experimental groups included the control group (no drug treatment), LPS group (cells stimulated with 5 μg/mL LPS for 48 hours to induce neuroinflammation), LPS+NC group (cells stimulated with LPS and transfected with an empty adenoviral vector), LPS+ Col4a2 Wt group (cells stimulated with LPS and transfected with the Col4a2 Wt -AdV vector), LPS+Col4a2 Mut group (cells stimulated with LPS and transfected with the Col4a2 Mut -AdV vector carrying the c.1838G>T, p.G613V mutation), and LPS+ Col4a2 Mut +WP1066 group (cells treated with the JAK2/STAT inhibitor WP1066 (5 μM, HY-15312; MCE, China) after stimulation with LPS and transfection with the Col4a2 Mut -AdV vector).

    Techniques: Mutagenesis, Activation Assay, Transfection, Plasmid Preparation, Fluorescence, Western Blot, Control