recombinant cytokines Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 97
    Thermo Fisher il 17a
    Il 17a, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17a/product/Thermo Fisher
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17a - by Bioz Stars, 2021-04
    97/100 stars
      Buy from Supplier

    86
    R&D Systems il 17
    Bleomycin-induced acute lung injury augments <t>IL-17</t> expression in alcohol-fed mice. Three-month-old wild-type mice were treated ± alcohol (20% v/v in drinking water for 8 weeks) before intratracheal administration of bleomycin (2.5 units/kg) or saline vehicle. Lungs were collected at 7 and 14 days following induction of injury and analyzed for IL-17 protein expression by Western blot. *p
    Il 17, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17/product/R&D Systems
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17 - by Bioz Stars, 2021-04
    86/100 stars
      Buy from Supplier

    86
    Thermo Fisher interleukin 10
    Rv1523 modulates macrophage immune responses. Overexpression of M. tuberculosis Rv1523 in M. smegmatis modulates the immune pathway by suppressing production of pro-inflammatory cytokine and inducing anti-inflammatory cytokine production. PMA-differentiated THP-1 cells (2 × 106/well/ml) were infected with recombinant Ms_Vec and Ms_Rv1523 strains. After 6, 24, and 48 h infection, the infected cells and supernatant were collected. ELISA was used for detecting the production of TNF-α (A) and <t>IL-10</t> (B) . Experiments were performed at least twice; SEM is represented by error bar for biological triplicates. Two-way ANOVA was used for determining statistical significance. ns, non-significant *p
    Interleukin 10, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/interleukin 10/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    interleukin 10 - by Bioz Stars, 2021-04
    86/100 stars
      Buy from Supplier

    93
    PeproTech il 17f
    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or <t>IL-17F</t> for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.
    Il 17f, supplied by PeproTech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17f/product/PeproTech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17f - by Bioz Stars, 2021-04
    93/100 stars
      Buy from Supplier

    N/A
    Recombinant human CKS 1 derived from E coli
      Buy from Supplier

    Image Search Results


    Bleomycin-induced acute lung injury augments IL-17 expression in alcohol-fed mice. Three-month-old wild-type mice were treated ± alcohol (20% v/v in drinking water for 8 weeks) before intratracheal administration of bleomycin (2.5 units/kg) or saline vehicle. Lungs were collected at 7 and 14 days following induction of injury and analyzed for IL-17 protein expression by Western blot. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: Bleomycin-induced acute lung injury augments IL-17 expression in alcohol-fed mice. Three-month-old wild-type mice were treated ± alcohol (20% v/v in drinking water for 8 weeks) before intratracheal administration of bleomycin (2.5 units/kg) or saline vehicle. Lungs were collected at 7 and 14 days following induction of injury and analyzed for IL-17 protein expression by Western blot. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Expressing, Mouse Assay, Western Blot

    Chronic alcohol ingestion increases the systemic Th17 immune response. CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old control-fed and alcohol-fed wild-type mice (20% v/v in drinking water for 8 weeks). ( A ) Cells were analyzed for IL-17 gene expression by quantitative PCR. CD4 + T cells harvested from control-fed and alcohol-fed animals were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours. ( B ) Cell culture supernatant was analyzed for IL-17 protein expression by ELISA. ( C ) Lastly, FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: Chronic alcohol ingestion increases the systemic Th17 immune response. CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old control-fed and alcohol-fed wild-type mice (20% v/v in drinking water for 8 weeks). ( A ) Cells were analyzed for IL-17 gene expression by quantitative PCR. CD4 + T cells harvested from control-fed and alcohol-fed animals were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours. ( B ) Cell culture supernatant was analyzed for IL-17 protein expression by ELISA. ( C ) Lastly, FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Mouse Assay, Expressing, Real-time Polymerase Chain Reaction, Ex Vivo, Cell Culture, Enzyme-linked Immunosorbent Assay, FACS, Isolation

    Chronic alcohol ingestion did not alter the CD4 + Th17 population in the lung. CD4 + T cells were isolated from the lung of three-month-old control-fed and alcohol-fed wild-type mice. FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. N = 3 per group. Data are presented as mean ± SEM.

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: Chronic alcohol ingestion did not alter the CD4 + Th17 population in the lung. CD4 + T cells were isolated from the lung of three-month-old control-fed and alcohol-fed wild-type mice. FACS analysis was performed on freshly isolated peripheral CD4 + T cells to determine the percentage of Th17 cells (CD4 + IL-17 + ). The right panel shows representative scattered dot plots. N = 3 per group. Data are presented as mean ± SEM.

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Isolation, Mouse Assay, FACS

    Alcohol exposure induces Th17 differentiation and enhances IL-17 production in both naïve CD4 + T helper cells (Th0) and Th17 cells in vitro . CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old wild-type mice. Naïve CD4 + T helper cells were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours (Th0). A subgroup of Th0 cells were activated and polarized with recombinant IL-6 (20 ng/ml) and recombinant TGFβ1 (5 ng/ml) for 72 hours to generate Th17 cells. Th0 and Th17 CD4 + T cells were cultured ± alcohol (60 mM) for 72 hours. The cell culture supernatant was collected and analyzed for IL-17 production by ELISA. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: Alcohol exposure induces Th17 differentiation and enhances IL-17 production in both naïve CD4 + T helper cells (Th0) and Th17 cells in vitro . CD4 + T cells were harvested from the spleen and lymph nodes of three-month-old wild-type mice. Naïve CD4 + T helper cells were activated ex vivo with anti-CD3 (5 μg/ml) and anti-CD28 (1 μg/ml) for 72 hours (Th0). A subgroup of Th0 cells were activated and polarized with recombinant IL-6 (20 ng/ml) and recombinant TGFβ1 (5 ng/ml) for 72 hours to generate Th17 cells. Th0 and Th17 CD4 + T cells were cultured ± alcohol (60 mM) for 72 hours. The cell culture supernatant was collected and analyzed for IL-17 production by ELISA. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: In Vitro, Mouse Assay, Ex Vivo, Recombinant, Cell Culture, Enzyme-linked Immunosorbent Assay

    IL-17 and TGFβ1 independently and additively inhibit lung fibroblast Thy-1 expression. Primary lung fibroblasts (PLFs from passage 3–8) were isolated from wild-type mice and cultured ± IL-17 (10 ng/ml) ± TGFβ1 (2 ng/ml) for 72 hours prior to analysis for Thy-1 by FACS. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: IL-17 and TGFβ1 independently and additively inhibit lung fibroblast Thy-1 expression. Primary lung fibroblasts (PLFs from passage 3–8) were isolated from wild-type mice and cultured ± IL-17 (10 ng/ml) ± TGFβ1 (2 ng/ml) for 72 hours prior to analysis for Thy-1 by FACS. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Expressing, Isolation, Mouse Assay, Cell Culture, FACS

    Thy-1 mediates the effects of IL-17 on α-SMA. Thy-1 subpopulations were enriched by immunomagnetic separation using the Miltenyi magnetic bead system. Thy-1 + and Thy-1 − PLFs were exposed to IL-17 (10 ng/ml) for 72 hours. Thy1 − PLFs (white bar (untreated) and dark gray bar (treated)) and Thy-1 + PLFs (black bar (untreated) and light gray bar (treated)) were harvested and then analyzed for α-SMA protein expression by Western blot. The top panel shows representative immunoblots. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: Thy-1 mediates the effects of IL-17 on α-SMA. Thy-1 subpopulations were enriched by immunomagnetic separation using the Miltenyi magnetic bead system. Thy-1 + and Thy-1 − PLFs were exposed to IL-17 (10 ng/ml) for 72 hours. Thy1 − PLFs (white bar (untreated) and dark gray bar (treated)) and Thy-1 + PLFs (black bar (untreated) and light gray bar (treated)) were harvested and then analyzed for α-SMA protein expression by Western blot. The top panel shows representative immunoblots. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Immunomagnetic Separation, Expressing, Western Blot

    IL-17 selectively induces myofibroblast stress fiber development in Thy-1 negative (Thy-1 − ) lung fibroblasts. Thy-1 + and Thy-1 − mouse PLFs were separately treated with IL-17 (10 ng/ml) or TGFβ1 (5 ng/ml) for 96 hours. Myofibroblast transdifferentiation was evaluated using immunofluorescent staining for α-SMA (green). DAPI (blue) was used for nuclear staining. Panels ( A - B ) show untreated Thy-1 + and Thy-1 − cells, respectively, ( C - D ) show Thy-1 + and Thy-1 − cells treated with IL-17, respectively, and ( E and F ) show Thy-1 + and Thy-1 − cells treated with TGFβ1, respectively. ( G ) Four random high-power fields from each sample were analyzed for stress fiber formation. Scale bar = 100 μm. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: IL-17 selectively induces myofibroblast stress fiber development in Thy-1 negative (Thy-1 − ) lung fibroblasts. Thy-1 + and Thy-1 − mouse PLFs were separately treated with IL-17 (10 ng/ml) or TGFβ1 (5 ng/ml) for 96 hours. Myofibroblast transdifferentiation was evaluated using immunofluorescent staining for α-SMA (green). DAPI (blue) was used for nuclear staining. Panels ( A - B ) show untreated Thy-1 + and Thy-1 − cells, respectively, ( C - D ) show Thy-1 + and Thy-1 − cells treated with IL-17, respectively, and ( E and F ) show Thy-1 + and Thy-1 − cells treated with TGFβ1, respectively. ( G ) Four random high-power fields from each sample were analyzed for stress fiber formation. Scale bar = 100 μm. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Staining

    IL-17 and alcohol upregulate α-SMA in lung fibroblasts. Total lung fibroblasts (Thy-1 + and Thy-1 − subpopulations) were exposed to either alcohol (60 mM) or IL-17 (10 ng/ml) for 72 hours. PLFs were harvested and then analyzed for α-SMA protein expression by Western blot. Untreated cells are represented by the white bar, alcohol-treated cells by the black bar, and IL-17-treated cells by the gray bar. The top panel shows a representative immunoblot. *p

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: IL-17 and alcohol upregulate α-SMA in lung fibroblasts. Total lung fibroblasts (Thy-1 + and Thy-1 − subpopulations) were exposed to either alcohol (60 mM) or IL-17 (10 ng/ml) for 72 hours. PLFs were harvested and then analyzed for α-SMA protein expression by Western blot. Untreated cells are represented by the white bar, alcohol-treated cells by the black bar, and IL-17-treated cells by the gray bar. The top panel shows a representative immunoblot. *p

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Expressing, Western Blot

    Hypothesis schematic showing the effects of IL-17 on myofibroblast development in chronic alcohol ingestion. In the current study, we showed that in the otherwise healthy animals, chronic alcohol ingestion increased systemic Th17 immune response. Acute injury caused a persistent increase in IL-17 in the lung. Alcohol, IL-17, and TGFβ1 independently inhibited Thy-1 expression by lung fibroblasts and IL-17 and TGFβ1 additively decreased Thy-1 expression leading to myofibroblast differentiation. We believe this sequence of events is one of the mechanisms by which alcohol induces fibroproliferative disrepair following acute lung injury.

    Journal: Alcoholism, clinical and experimental research

    Article Title: Alcohol-induced interleukin-17 expression causes murine lung fibroblast-to-myofibroblast transdifferentiation via Thy-1 downregulation

    doi: 10.1111/acer.14110

    Figure Lengend Snippet: Hypothesis schematic showing the effects of IL-17 on myofibroblast development in chronic alcohol ingestion. In the current study, we showed that in the otherwise healthy animals, chronic alcohol ingestion increased systemic Th17 immune response. Acute injury caused a persistent increase in IL-17 in the lung. Alcohol, IL-17, and TGFβ1 independently inhibited Thy-1 expression by lung fibroblasts and IL-17 and TGFβ1 additively decreased Thy-1 expression leading to myofibroblast differentiation. We believe this sequence of events is one of the mechanisms by which alcohol induces fibroproliferative disrepair following acute lung injury.

    Article Snippet: Cells were treated with either alcohol (60 mM), TGFβ1 (2 ng/ml; R & D Systems, Minneapolis, MN), or IL-17 (10 ng/ml; R & D Systems).

    Techniques: Expressing, Sequencing

    Rv1523 modulates macrophage immune responses. Overexpression of M. tuberculosis Rv1523 in M. smegmatis modulates the immune pathway by suppressing production of pro-inflammatory cytokine and inducing anti-inflammatory cytokine production. PMA-differentiated THP-1 cells (2 × 106/well/ml) were infected with recombinant Ms_Vec and Ms_Rv1523 strains. After 6, 24, and 48 h infection, the infected cells and supernatant were collected. ELISA was used for detecting the production of TNF-α (A) and IL-10 (B) . Experiments were performed at least twice; SEM is represented by error bar for biological triplicates. Two-way ANOVA was used for determining statistical significance. ns, non-significant *p

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: The M. tuberculosis Rv1523 Methyltransferase Promotes Drug Resistance Through Methylation-Mediated Cell Wall Remodeling and Modulates Macrophages Immune Responses

    doi: 10.3389/fcimb.2021.622487

    Figure Lengend Snippet: Rv1523 modulates macrophage immune responses. Overexpression of M. tuberculosis Rv1523 in M. smegmatis modulates the immune pathway by suppressing production of pro-inflammatory cytokine and inducing anti-inflammatory cytokine production. PMA-differentiated THP-1 cells (2 × 106/well/ml) were infected with recombinant Ms_Vec and Ms_Rv1523 strains. After 6, 24, and 48 h infection, the infected cells and supernatant were collected. ELISA was used for detecting the production of TNF-α (A) and IL-10 (B) . Experiments were performed at least twice; SEM is represented by error bar for biological triplicates. Two-way ANOVA was used for determining statistical significance. ns, non-significant *p

    Article Snippet: After 6, 24, and 48 h infection, culture supernatants were harvested, and the cytokines released by infected cells in the culture supernatants were quantitatively detected using ELISA kits of Tumor Necrosis Factor-α (TNF-α Invitrogen™ 88-7346-88) and interleukin-10 (IL-10 Invitrogen™ 88-7106-88).

    Techniques: Over Expression, Infection, Recombinant, Enzyme-linked Immunosorbent Assay

    Model depicting the role of Rv1523 in bacterial cell wall lipid modulation and macrophages immune response alteration. We predict the role of Rv1523 methyltransferase in cell wall lipid modulation. Recombinant M. smegmatis expressing Rv1523 (Ms_Rv1523) displayed higher survival in macrophages as compared to M. smegmatis not expressing Rv1523 (Ms_Vec). Ms_Rv1523 induced increased expression of anti-inflammatory cytokine IL-10 and reduced the expression of proinflammatory TNF- α.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: The M. tuberculosis Rv1523 Methyltransferase Promotes Drug Resistance Through Methylation-Mediated Cell Wall Remodeling and Modulates Macrophages Immune Responses

    doi: 10.3389/fcimb.2021.622487

    Figure Lengend Snippet: Model depicting the role of Rv1523 in bacterial cell wall lipid modulation and macrophages immune response alteration. We predict the role of Rv1523 methyltransferase in cell wall lipid modulation. Recombinant M. smegmatis expressing Rv1523 (Ms_Rv1523) displayed higher survival in macrophages as compared to M. smegmatis not expressing Rv1523 (Ms_Vec). Ms_Rv1523 induced increased expression of anti-inflammatory cytokine IL-10 and reduced the expression of proinflammatory TNF- α.

    Article Snippet: After 6, 24, and 48 h infection, culture supernatants were harvested, and the cytokines released by infected cells in the culture supernatants were quantitatively detected using ELISA kits of Tumor Necrosis Factor-α (TNF-α Invitrogen™ 88-7346-88) and interleukin-10 (IL-10 Invitrogen™ 88-7106-88).

    Techniques: Recombinant, Expressing

    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: shRNA, Activation Assay, In Vitro, Infection, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Standard Deviation, Negative Control

    IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: Activation Assay, In Vitro, Recombinant, Enzyme-linked Immunosorbent Assay, Expressing, Marker, Western Blot, Standard Deviation

    Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: Activation Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, shRNA, Negative Control