il 17░a  (PeproTech)

 
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    Name:
    Anti Human IL 17 IL 17A
    Description:
    Rabbit Anti Human IL 17A Source Polyclonal Rabbit Formulation Lyophilized Produced from sera of rabbits pre immunized with highly pure 98 recombinant hIL 17A Anti Human IL 17A specific antibody was purified by affinity chromatography employing immobilized hIL 17 matrix
    Catalog Number:
    500-P07-100UG
    Price:
    250.00
    Category:
    Antibodies
    Source:
    Polyclonal Rabbit
    Quantity:
    100UG
    Buy from Supplier


    Structured Review

    PeproTech il 17░a
    <t>IL-17░A</t> promoted the migration and invasion of NSCLC cells in vitro . The migration activities of A549 ( A ) and H460 ( B ) cells, and the invasion activities of A549 ( C ) and H460 ( D ) cells before and after treatment of rhIL-17░A was analyzed using transwell assay. One representative analysis is shown. Data are presented as a histogram. ( E) The expression of N-cadherin in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. ( F) The relative expression of N-cadherin in A549 and H460 cells before and after treatment with rhIL-17░A was analyzed using qPCR. (G) The expressions of IL-17░A and CD31 in tumor tissues from NSCLC patients were detected by immunofluorescence. * indicates P
    Rabbit Anti Human IL 17A Source Polyclonal Rabbit Formulation Lyophilized Produced from sera of rabbits pre immunized with highly pure 98 recombinant hIL 17A Anti Human IL 17A specific antibody was purified by affinity chromatography employing immobilized hIL 17 matrix
    https://www.bioz.com/result/il 17░a/product/PeproTech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17░a - by Bioz Stars, 2021-06
    93/100 stars

    Images

    1) Product Images from "Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer"

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

    Journal: Oncoimmunology

    doi: 10.1080/2162402X.2018.1461303

    IL-17░A promoted the migration and invasion of NSCLC cells in vitro . The migration activities of A549 ( A ) and H460 ( B ) cells, and the invasion activities of A549 ( C ) and H460 ( D ) cells before and after treatment of rhIL-17░A was analyzed using transwell assay. One representative analysis is shown. Data are presented as a histogram. ( E) The expression of N-cadherin in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. ( F) The relative expression of N-cadherin in A549 and H460 cells before and after treatment with rhIL-17░A was analyzed using qPCR. (G) The expressions of IL-17░A and CD31 in tumor tissues from NSCLC patients were detected by immunofluorescence. * indicates P
    Figure Legend Snippet: IL-17░A promoted the migration and invasion of NSCLC cells in vitro . The migration activities of A549 ( A ) and H460 ( B ) cells, and the invasion activities of A549 ( C ) and H460 ( D ) cells before and after treatment of rhIL-17░A was analyzed using transwell assay. One representative analysis is shown. Data are presented as a histogram. ( E) The expression of N-cadherin in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. ( F) The relative expression of N-cadherin in A549 and H460 cells before and after treatment with rhIL-17░A was analyzed using qPCR. (G) The expressions of IL-17░A and CD31 in tumor tissues from NSCLC patients were detected by immunofluorescence. * indicates P

    Techniques Used: Migration, In Vitro, Transwell Assay, Expressing, Western Blot, Real-time Polymerase Chain Reaction, Immunofluorescence

    The level of Th17 cells was associated with poor survival in NSCLC patients. The relationship between Th17 frequency and TNM stage ( A ), tumor grade ( B ) and lymph node metastasis ( C ) of NSCLC patients, respectively. The changes of Th17 cell frequency in peripheral blood from NSCLC patients before and after chemotherapy with the status of PD ( D ), PR ( E ) and SD ( F ). ( G) IL-17░A expression in tumor tissues of NSCLC was analyzed by immunohistochemistry. ( H) Kaplan-Meier survival curves for NSCLC patients with lower and higher IL-17░A expression (immunohistochemistry analysis). *, ** and ns indicate P
    Figure Legend Snippet: The level of Th17 cells was associated with poor survival in NSCLC patients. The relationship between Th17 frequency and TNM stage ( A ), tumor grade ( B ) and lymph node metastasis ( C ) of NSCLC patients, respectively. The changes of Th17 cell frequency in peripheral blood from NSCLC patients before and after chemotherapy with the status of PD ( D ), PR ( E ) and SD ( F ). ( G) IL-17░A expression in tumor tissues of NSCLC was analyzed by immunohistochemistry. ( H) Kaplan-Meier survival curves for NSCLC patients with lower and higher IL-17░A expression (immunohistochemistry analysis). *, ** and ns indicate P

    Techniques Used: Expressing, Immunohistochemistry

    IL-17░A promoted the CSC-like properties of NSCLC cells. A549 ( A ) and H460 ( B ) cells were cultured with rhIL-17░A for 7 days, and then collected for sphere assay. One representative photomicrograph is shown. Data are presented as a histogram. ( C) The expression of Oct4 in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. The apoptosis of A549 ( D ) and H460 ( E ) cells treated with or without docetaxel and rhIL-17░A was analyzed by flow cytometry. IL-17░A expression in IL-17░A-expressing and control vectors-tranfected H460 cells was analyzed by western blotting ( F ) and qPCR ( G ). ( H) IL-17░A promotes NSCLC tumor growth in vivo . IL-17░A expressing A549 cells were injected subcutaneously into nude mice (n = 6 mice/group). Tumor volumes were measured at 21 days after cell implantation. ( I) Lump images of xenograft tumors that were formed in nude mice at 21 days after cell implantation. ( J) The result of tumor weights at 21 days after cell implantation was shown as histogram. ( K) Tumor growth curve from 7 to 21 days after cell implantation was shown as statistical graph. * indicates P
    Figure Legend Snippet: IL-17░A promoted the CSC-like properties of NSCLC cells. A549 ( A ) and H460 ( B ) cells were cultured with rhIL-17░A for 7 days, and then collected for sphere assay. One representative photomicrograph is shown. Data are presented as a histogram. ( C) The expression of Oct4 in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. The apoptosis of A549 ( D ) and H460 ( E ) cells treated with or without docetaxel and rhIL-17░A was analyzed by flow cytometry. IL-17░A expression in IL-17░A-expressing and control vectors-tranfected H460 cells was analyzed by western blotting ( F ) and qPCR ( G ). ( H) IL-17░A promotes NSCLC tumor growth in vivo . IL-17░A expressing A549 cells were injected subcutaneously into nude mice (n = 6 mice/group). Tumor volumes were measured at 21 days after cell implantation. ( I) Lump images of xenograft tumors that were formed in nude mice at 21 days after cell implantation. ( J) The result of tumor weights at 21 days after cell implantation was shown as histogram. ( K) Tumor growth curve from 7 to 21 days after cell implantation was shown as statistical graph. * indicates P

    Techniques Used: Cell Culture, Expressing, Western Blot, Flow Cytometry, Cytometry, Real-time Polymerase Chain Reaction, In Vivo, Injection, Mouse Assay

    Blockade of STAT3/NF-κB/Notch1 signaling inhibited NSCLC stemness promoted by IL-17░A. (A) After the treatment with STAT3░or NF-κB or Notch1 inhibitor, the sphere forming of A549 and H460 cells induce by rhIL-17░A was blocked. One representative photomicrograph is shown. The results from A549 ( B ) and H460 ( C ) cells were shown as histogram. ( D) The expression of Oct4 in A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by western blotting. The apoptosis of A549 ( E ) and H460 ( F ) cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. * indicates P
    Figure Legend Snippet: Blockade of STAT3/NF-κB/Notch1 signaling inhibited NSCLC stemness promoted by IL-17░A. (A) After the treatment with STAT3░or NF-κB or Notch1 inhibitor, the sphere forming of A549 and H460 cells induce by rhIL-17░A was blocked. One representative photomicrograph is shown. The results from A549 ( B ) and H460 ( C ) cells were shown as histogram. ( D) The expression of Oct4 in A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by western blotting. The apoptosis of A549 ( E ) and H460 ( F ) cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. * indicates P

    Techniques Used: Expressing, Western Blot, Transwell Assay

    The STAT3/NF-κB/Notch1 signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. ( B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 ( C ) and H460 ( D ) cells are presented as histogram. ( E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 ( F ) and H460 ( G ) cells are presented as a histogram. ( H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P
    Figure Legend Snippet: The STAT3/NF-κB/Notch1 signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. ( B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 ( C ) and H460 ( D ) cells are presented as histogram. ( E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 ( F ) and H460 ( G ) cells are presented as a histogram. ( H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P

    Techniques Used: Migration, Activation Assay, Western Blot, Transwell Assay, Expressing

    Related Articles

    Staining:

    Article Title: Inflammatory and degenerative phases resulting from anterior cruciate rupture in a non‐invasive murine model of post‐traumatic osteoarthritis
    Article Snippet: .. Low power images of sections taken from uninjured and injured legs at day‐3, 14 and −21 stained with antibodies to IL‐6 and IL‐17A. ..

    SDS Page:

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer
    Article Snippet: Quantified protein lysates were measured with a Protein BCA Assay Kit (Thermo Fisher, #23228) according to the manufacturer's instructions. .. The proteins in lysates were resolved on SDS-PAGE gels, transferred onto PVDF membranes (Millipore, #ISEEQ00010), and immunoblotted with anti-human N-cadherin (Cell signaling Technology, #13116), snail (Cell signaling Technology, #3879), vimentin (Cell signaling Technology, #5741), p-STAT3 (Cell signaling Technology, #9145), p-p65 (Cell signaling Technology, #3033), cleaved-Notch1 (Cell signaling Technology, #4147), Oct4 (Cell signaling Technology, #2750), Nanog (Cell signaling Technology, #4903), Sox2 (Cell signaling Technology, #3579), IL-17░A (PeproTech, #500-P07) and anti-human β-actin antibody (ProteinTech, #20536-1-AP-50). .. For detecting IL-17░A mRNA level in peripheral blood, total RNA was extracted from PBMC of healthy donors and NSCLC patients by TRIzol reagent (Takara, #9109) according to the manufacturer's instructions.. For detection of IL-17░A and IL-17R mRNA in tissues, total RNA was extracted from tumor tissues and non-tumor tissues of NSCLC patients.

    other:

    Article Title: Inflammatory and degenerative phases resulting from anterior cruciate rupture in a non‐invasive murine model of post‐traumatic osteoarthritis
    Article Snippet: Primary antibodies: Rat monoclonal to F4/80 (clone Cl:A3‐1; AbD Serotec®, Biorad, Kidlington, UK), rabbit monoclonal to Cd11b (clone EPR1344; Abcam, Cambridge, UK), rabbit polyclonal to IL‐6 (Novusbio Biotechne, Abingdon, UK), Rabbit polyclonal to IL‐17A (Peprotech, London, UK).

    Article Title: Comparison of three different ELISAs for the detection of recombinant, native and plasma IL-17A
    Article Snippet: Here, we demonstrate that the eBio64CAP17 neutralizing mAb and the 500-P07G polyclonal Ab are reliable to capture IL-17A in sandwich ELISAs.

    Article Title: Protein Kinase Serine/Threonine Kinase 24 Positively Regulates Interleukin 17-Induced Inflammation by Promoting IKK Complex Activation
    Article Snippet: Reagents and AntibodiesRecombinant IL-17A (mouse and human) were purchased from PeproTech (PeproTech, Rocky Hill, NJ, USA); human IL-17F (11855-HNAE), IL-1β, and TNF-α were purchased from Sino Biological Inc.; Primary antibodies against P-P65 (3033S), P-P38 (4511S), P-ERK1/2 (4370S), P-JNK (9251S), P-IκBα (2859), P-IKKα/β (2697), P-TAK1 (4508), IκBα (4814), P65 (8242), P38 (8690), and ERK1/2 (4695) were purchased from Cell Signaling Technology.

    Recombinant:

    Article Title: Lack of FGF21 promotes NASH-HCC transition via hepatocyte-TLR4-IL-17A signaling
    Article Snippet: Then hepatocytes and splenocytes were co-cultured, without refreshing the medium, for 72 h. For FFA challenging, palmic acid (PA) (Sigma-Aldrich, USA) at 100 uM was used to treat the cells, and 1% BSA was used as treatment control. .. To determine the effects of FGF21 and IL-17A antibody on cells, Recombinant Human FGF-21 (#100-42; PeproTech; Rocky Hill, NJ, USA) was used at 100 ng/mL, lipopolysaccharide (LPS, from Escherichia coli, Sigma Aldrich, USA) at 1 µg/mL, (-)-parthenolide (#S2341, Selleckchem, TX, USA) at 100 ng/mL, and InVivoMAb anti-mouse IL-17A (#BE0173, clone 17F3, Bio X Cell, Lebanon) was used at 100 ng/mL to treat cell for 24 h. An assay was performed to co-culture indirectly the 3T3-L1 cells with the benign and malignant hepatic cell lines (Hepa1-6 cells, FL83B cells, Hepa1-6-21KD cells and FL83B-21KD cells) using a Transwell plate. .. In brief, 3T3-L1 cells were differentiated up to 8 days, and then seeded at 1 × 105 in the insert of Trans-well plate for 24 h. After treatment with lipopolysaccharide LPS (Sigma Aldrich, USA) at 1 µg/mL for 12 h, the 3T3-L1 cells were co-cultured with hepatic cells for additional 24 h.

    Co-Culture Assay:

    Article Title: Lack of FGF21 promotes NASH-HCC transition via hepatocyte-TLR4-IL-17A signaling
    Article Snippet: Then hepatocytes and splenocytes were co-cultured, without refreshing the medium, for 72 h. For FFA challenging, palmic acid (PA) (Sigma-Aldrich, USA) at 100 uM was used to treat the cells, and 1% BSA was used as treatment control. .. To determine the effects of FGF21 and IL-17A antibody on cells, Recombinant Human FGF-21 (#100-42; PeproTech; Rocky Hill, NJ, USA) was used at 100 ng/mL, lipopolysaccharide (LPS, from Escherichia coli, Sigma Aldrich, USA) at 1 µg/mL, (-)-parthenolide (#S2341, Selleckchem, TX, USA) at 100 ng/mL, and InVivoMAb anti-mouse IL-17A (#BE0173, clone 17F3, Bio X Cell, Lebanon) was used at 100 ng/mL to treat cell for 24 h. An assay was performed to co-culture indirectly the 3T3-L1 cells with the benign and malignant hepatic cell lines (Hepa1-6 cells, FL83B cells, Hepa1-6-21KD cells and FL83B-21KD cells) using a Transwell plate. .. In brief, 3T3-L1 cells were differentiated up to 8 days, and then seeded at 1 × 105 in the insert of Trans-well plate for 24 h. After treatment with lipopolysaccharide LPS (Sigma Aldrich, USA) at 1 µg/mL for 12 h, the 3T3-L1 cells were co-cultured with hepatic cells for additional 24 h.

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  • Bioz Stars
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  • 93
    PeproTech il 17░a
    <t>IL-17░A</t> promoted the migration and invasion of NSCLC cells in vitro . The migration activities of A549 ( A ) and H460 ( B ) cells, and the invasion activities of A549 ( C ) and H460 ( D ) cells before and after treatment of rhIL-17░A was analyzed using transwell assay. One representative analysis is shown. Data are presented as a histogram. ( E) The expression of N-cadherin in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. ( F) The relative expression of N-cadherin in A549 and H460 cells before and after treatment with rhIL-17░A was analyzed using qPCR. (G) The expressions of IL-17░A and CD31 in tumor tissues from NSCLC patients were detected by immunofluorescence. * indicates P
    Il 17░A, 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 17░a/product/PeproTech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17░a - by Bioz Stars, 2021-06
    93/100 stars
      Buy from Supplier

    96
    PeproTech recombinant murine il 17a
    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 <t>IL-17A</t> 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.
    Recombinant Murine Il 17a, supplied by PeproTech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant murine il 17a/product/PeproTech
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant murine il 17a - by Bioz Stars, 2021-06
    96/100 stars
      Buy from Supplier

    Image Search Results


    IL-17░A promoted the migration and invasion of NSCLC cells in vitro . The migration activities of A549 ( A ) and H460 ( B ) cells, and the invasion activities of A549 ( C ) and H460 ( D ) cells before and after treatment of rhIL-17░A was analyzed using transwell assay. One representative analysis is shown. Data are presented as a histogram. ( E) The expression of N-cadherin in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. ( F) The relative expression of N-cadherin in A549 and H460 cells before and after treatment with rhIL-17░A was analyzed using qPCR. (G) The expressions of IL-17░A and CD31 in tumor tissues from NSCLC patients were detected by immunofluorescence. * indicates P

    Journal: Oncoimmunology

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

    doi: 10.1080/2162402X.2018.1461303

    Figure Lengend Snippet: IL-17░A promoted the migration and invasion of NSCLC cells in vitro . The migration activities of A549 ( A ) and H460 ( B ) cells, and the invasion activities of A549 ( C ) and H460 ( D ) cells before and after treatment of rhIL-17░A was analyzed using transwell assay. One representative analysis is shown. Data are presented as a histogram. ( E) The expression of N-cadherin in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. ( F) The relative expression of N-cadherin in A549 and H460 cells before and after treatment with rhIL-17░A was analyzed using qPCR. (G) The expressions of IL-17░A and CD31 in tumor tissues from NSCLC patients were detected by immunofluorescence. * indicates P

    Article Snippet: The proteins in lysates were resolved on SDS-PAGE gels, transferred onto PVDF membranes (Millipore, #ISEEQ00010), and immunoblotted with anti-human N-cadherin (Cell signaling Technology, #13116), snail (Cell signaling Technology, #3879), vimentin (Cell signaling Technology, #5741), p-STAT3 (Cell signaling Technology, #9145), p-p65 (Cell signaling Technology, #3033), cleaved-Notch1 (Cell signaling Technology, #4147), Oct4 (Cell signaling Technology, #2750), Nanog (Cell signaling Technology, #4903), Sox2 (Cell signaling Technology, #3579), IL-17░A (PeproTech, #500-P07) and anti-human β-actin antibody (ProteinTech, #20536-1-AP-50).

    Techniques: Migration, In Vitro, Transwell Assay, Expressing, Western Blot, Real-time Polymerase Chain Reaction, Immunofluorescence

    The level of Th17 cells was associated with poor survival in NSCLC patients. The relationship between Th17 frequency and TNM stage ( A ), tumor grade ( B ) and lymph node metastasis ( C ) of NSCLC patients, respectively. The changes of Th17 cell frequency in peripheral blood from NSCLC patients before and after chemotherapy with the status of PD ( D ), PR ( E ) and SD ( F ). ( G) IL-17░A expression in tumor tissues of NSCLC was analyzed by immunohistochemistry. ( H) Kaplan-Meier survival curves for NSCLC patients with lower and higher IL-17░A expression (immunohistochemistry analysis). *, ** and ns indicate P

    Journal: Oncoimmunology

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

    doi: 10.1080/2162402X.2018.1461303

    Figure Lengend Snippet: The level of Th17 cells was associated with poor survival in NSCLC patients. The relationship between Th17 frequency and TNM stage ( A ), tumor grade ( B ) and lymph node metastasis ( C ) of NSCLC patients, respectively. The changes of Th17 cell frequency in peripheral blood from NSCLC patients before and after chemotherapy with the status of PD ( D ), PR ( E ) and SD ( F ). ( G) IL-17░A expression in tumor tissues of NSCLC was analyzed by immunohistochemistry. ( H) Kaplan-Meier survival curves for NSCLC patients with lower and higher IL-17░A expression (immunohistochemistry analysis). *, ** and ns indicate P

    Article Snippet: The proteins in lysates were resolved on SDS-PAGE gels, transferred onto PVDF membranes (Millipore, #ISEEQ00010), and immunoblotted with anti-human N-cadherin (Cell signaling Technology, #13116), snail (Cell signaling Technology, #3879), vimentin (Cell signaling Technology, #5741), p-STAT3 (Cell signaling Technology, #9145), p-p65 (Cell signaling Technology, #3033), cleaved-Notch1 (Cell signaling Technology, #4147), Oct4 (Cell signaling Technology, #2750), Nanog (Cell signaling Technology, #4903), Sox2 (Cell signaling Technology, #3579), IL-17░A (PeproTech, #500-P07) and anti-human β-actin antibody (ProteinTech, #20536-1-AP-50).

    Techniques: Expressing, Immunohistochemistry

    IL-17░A promoted the CSC-like properties of NSCLC cells. A549 ( A ) and H460 ( B ) cells were cultured with rhIL-17░A for 7 days, and then collected for sphere assay. One representative photomicrograph is shown. Data are presented as a histogram. ( C) The expression of Oct4 in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. The apoptosis of A549 ( D ) and H460 ( E ) cells treated with or without docetaxel and rhIL-17░A was analyzed by flow cytometry. IL-17░A expression in IL-17░A-expressing and control vectors-tranfected H460 cells was analyzed by western blotting ( F ) and qPCR ( G ). ( H) IL-17░A promotes NSCLC tumor growth in vivo . IL-17░A expressing A549 cells were injected subcutaneously into nude mice (n = 6 mice/group). Tumor volumes were measured at 21 days after cell implantation. ( I) Lump images of xenograft tumors that were formed in nude mice at 21 days after cell implantation. ( J) The result of tumor weights at 21 days after cell implantation was shown as histogram. ( K) Tumor growth curve from 7 to 21 days after cell implantation was shown as statistical graph. * indicates P

    Journal: Oncoimmunology

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

    doi: 10.1080/2162402X.2018.1461303

    Figure Lengend Snippet: IL-17░A promoted the CSC-like properties of NSCLC cells. A549 ( A ) and H460 ( B ) cells were cultured with rhIL-17░A for 7 days, and then collected for sphere assay. One representative photomicrograph is shown. Data are presented as a histogram. ( C) The expression of Oct4 in A549 and H460 cells before and after treatment of rhIL-17░A was analyzed using western blotting. The apoptosis of A549 ( D ) and H460 ( E ) cells treated with or without docetaxel and rhIL-17░A was analyzed by flow cytometry. IL-17░A expression in IL-17░A-expressing and control vectors-tranfected H460 cells was analyzed by western blotting ( F ) and qPCR ( G ). ( H) IL-17░A promotes NSCLC tumor growth in vivo . IL-17░A expressing A549 cells were injected subcutaneously into nude mice (n = 6 mice/group). Tumor volumes were measured at 21 days after cell implantation. ( I) Lump images of xenograft tumors that were formed in nude mice at 21 days after cell implantation. ( J) The result of tumor weights at 21 days after cell implantation was shown as histogram. ( K) Tumor growth curve from 7 to 21 days after cell implantation was shown as statistical graph. * indicates P

    Article Snippet: The proteins in lysates were resolved on SDS-PAGE gels, transferred onto PVDF membranes (Millipore, #ISEEQ00010), and immunoblotted with anti-human N-cadherin (Cell signaling Technology, #13116), snail (Cell signaling Technology, #3879), vimentin (Cell signaling Technology, #5741), p-STAT3 (Cell signaling Technology, #9145), p-p65 (Cell signaling Technology, #3033), cleaved-Notch1 (Cell signaling Technology, #4147), Oct4 (Cell signaling Technology, #2750), Nanog (Cell signaling Technology, #4903), Sox2 (Cell signaling Technology, #3579), IL-17░A (PeproTech, #500-P07) and anti-human β-actin antibody (ProteinTech, #20536-1-AP-50).

    Techniques: Cell Culture, Expressing, Western Blot, Flow Cytometry, Cytometry, Real-time Polymerase Chain Reaction, In Vivo, Injection, Mouse Assay

    Blockade of STAT3/NF-κB/Notch1 signaling inhibited NSCLC stemness promoted by IL-17░A. (A) After the treatment with STAT3░or NF-κB or Notch1 inhibitor, the sphere forming of A549 and H460 cells induce by rhIL-17░A was blocked. One representative photomicrograph is shown. The results from A549 ( B ) and H460 ( C ) cells were shown as histogram. ( D) The expression of Oct4 in A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by western blotting. The apoptosis of A549 ( E ) and H460 ( F ) cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. * indicates P

    Journal: Oncoimmunology

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

    doi: 10.1080/2162402X.2018.1461303

    Figure Lengend Snippet: Blockade of STAT3/NF-κB/Notch1 signaling inhibited NSCLC stemness promoted by IL-17░A. (A) After the treatment with STAT3░or NF-κB or Notch1 inhibitor, the sphere forming of A549 and H460 cells induce by rhIL-17░A was blocked. One representative photomicrograph is shown. The results from A549 ( B ) and H460 ( C ) cells were shown as histogram. ( D) The expression of Oct4 in A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by western blotting. The apoptosis of A549 ( E ) and H460 ( F ) cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. * indicates P

    Article Snippet: The proteins in lysates were resolved on SDS-PAGE gels, transferred onto PVDF membranes (Millipore, #ISEEQ00010), and immunoblotted with anti-human N-cadherin (Cell signaling Technology, #13116), snail (Cell signaling Technology, #3879), vimentin (Cell signaling Technology, #5741), p-STAT3 (Cell signaling Technology, #9145), p-p65 (Cell signaling Technology, #3033), cleaved-Notch1 (Cell signaling Technology, #4147), Oct4 (Cell signaling Technology, #2750), Nanog (Cell signaling Technology, #4903), Sox2 (Cell signaling Technology, #3579), IL-17░A (PeproTech, #500-P07) and anti-human β-actin antibody (ProteinTech, #20536-1-AP-50).

    Techniques: Expressing, Western Blot, Transwell Assay

    The STAT3/NF-κB/Notch1 signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. ( B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 ( C ) and H460 ( D ) cells are presented as histogram. ( E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 ( F ) and H460 ( G ) cells are presented as a histogram. ( H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P

    Journal: Oncoimmunology

    Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

    doi: 10.1080/2162402X.2018.1461303

    Figure Lengend Snippet: The STAT3/NF-κB/Notch1 signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. ( B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 ( C ) and H460 ( D ) cells are presented as histogram. ( E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 ( F ) and H460 ( G ) cells are presented as a histogram. ( H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P

    Article Snippet: The proteins in lysates were resolved on SDS-PAGE gels, transferred onto PVDF membranes (Millipore, #ISEEQ00010), and immunoblotted with anti-human N-cadherin (Cell signaling Technology, #13116), snail (Cell signaling Technology, #3879), vimentin (Cell signaling Technology, #5741), p-STAT3 (Cell signaling Technology, #9145), p-p65 (Cell signaling Technology, #3033), cleaved-Notch1 (Cell signaling Technology, #4147), Oct4 (Cell signaling Technology, #2750), Nanog (Cell signaling Technology, #4903), Sox2 (Cell signaling Technology, #3579), IL-17░A (PeproTech, #500-P07) and anti-human β-actin antibody (ProteinTech, #20536-1-AP-50).

    Techniques: Migration, Activation Assay, Western Blot, Transwell Assay, 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

    Release of IL-18 in splenocytes from ICE KO mice. Splenocytes from WT or ICE KO mice were cultured for 24 hours in the absence of any exogenous stimulation. IL-18 levels were measured in supernatants. Data are mean ± SEM of 8 mice per group. ** P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Release of IL-18 in splenocytes from ICE KO mice. Splenocytes from WT or ICE KO mice were cultured for 24 hours in the absence of any exogenous stimulation. IL-18 levels were measured in supernatants. Data are mean ± SEM of 8 mice per group. ** P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Mouse Assay, Cell Culture

    Constitutive expression of pro–IL-18 in the spleens and livers on untreated mice. Spleen and liver homogenates from 3 untreated mice were subjected to Western blot analysis with a specific rabbit anti-murine IL-18 antiserum. Recombinant murine pro–IL-18 and mature IL-18 were used as standards.

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Constitutive expression of pro–IL-18 in the spleens and livers on untreated mice. Spleen and liver homogenates from 3 untreated mice were subjected to Western blot analysis with a specific rabbit anti-murine IL-18 antiserum. Recombinant murine pro–IL-18 and mature IL-18 were used as standards.

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Expressing, Mouse Assay, Western Blot, Recombinant

    Increase in serum IL-18 levels after IL-12 administration. WT and ICE KO mice received 4 daily intraperitoneal injections of IL-12 (100 or 400 ng/mouse) or vehicle. Two hours after the fourth injection, blood was collected and serum was prepared. Data are mean ± SEM of 10 mice per group. * P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Increase in serum IL-18 levels after IL-12 administration. WT and ICE KO mice received 4 daily intraperitoneal injections of IL-12 (100 or 400 ng/mouse) or vehicle. Two hours after the fourth injection, blood was collected and serum was prepared. Data are mean ± SEM of 10 mice per group. * P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Mouse Assay, Injection

    Neutralization of IL-18 reduces IL-12–induced IFN-γ levels in vivo. Mice received 4 daily intraperitoneal injections of IL-12 (100 ng/mouse). One hour before the first and the third injection, the antibody-treated group received an intraperitoneal injection of 200 μL of rabbit anti–IL-18 antiserum, whereas the control group received the same amount of NRS. Two hours after the fourth injection, blood was collected and serum was prepared for measurement of IFN-γ. Data are mean ± SEM of 5 mice per group. ** P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Neutralization of IL-18 reduces IL-12–induced IFN-γ levels in vivo. Mice received 4 daily intraperitoneal injections of IL-12 (100 ng/mouse). One hour before the first and the third injection, the antibody-treated group received an intraperitoneal injection of 200 μL of rabbit anti–IL-18 antiserum, whereas the control group received the same amount of NRS. Two hours after the fourth injection, blood was collected and serum was prepared for measurement of IFN-γ. Data are mean ± SEM of 5 mice per group. ** P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Neutralization, In Vivo, Mouse Assay, Injection

    IL-18 production in unstimulated and IL-12–stimulated splenocytes. Splenocytes were cultured in RPMI-FBS for increasing amounts of time without added exogenous stimulation, or with IL-12 at 10 ng/mL. Cell-associated and released IL-18 levels were measured. Data are mean ± SEM of 9 mice per group.

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: IL-18 production in unstimulated and IL-12–stimulated splenocytes. Splenocytes were cultured in RPMI-FBS for increasing amounts of time without added exogenous stimulation, or with IL-12 at 10 ng/mL. Cell-associated and released IL-18 levels were measured. Data are mean ± SEM of 9 mice per group.

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Cell Culture, Mouse Assay

    Effect of IL-18 neutralization on the induction of IFN-γ by IL-12 in vitro. Splenocytes were cultured for 48 hours with increasing concentrations of IL-12 (0.1–10 ng/mL) in the presence or absence of either neutralizing anti–IL-18 IgG or control IgG (50 μg/mL). IFN-γ levels were measured in the supernatants. Data are mean ± SEM of 3 mice per group and are representative of 1 experiment out of 3 performed. * P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Effect of IL-18 neutralization on the induction of IFN-γ by IL-12 in vitro. Splenocytes were cultured for 48 hours with increasing concentrations of IL-12 (0.1–10 ng/mL) in the presence or absence of either neutralizing anti–IL-18 IgG or control IgG (50 μg/mL). IFN-γ levels were measured in the supernatants. Data are mean ± SEM of 3 mice per group and are representative of 1 experiment out of 3 performed. * P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Neutralization, In Vitro, Cell Culture, Mouse Assay

    Short hairpin RNA design, interference efficiency assay, and lentivirus transduction. A: DNA sequence analysis of pGCSIL/Interleukin-17A receptor (IL-17RA) short hairpin RNA (shRNA) 1; B: Lentiviral-mediated IL-17RA shRNA 1, 2, 3, and 4 (shRNA 1, 2, 3, and 4) inhibited IL-17RA mRNA expression in hepatic stellate cells (HSCs). HSCs infected with lentivirus at a multiplicity of infection of 10 for 72 h, and IL-17RA mRNA expression was quantified by polymerase chain reaction. IL-17RA shRNA 1 was the most efficient silencing tool for IL-17RA. b P

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    doi: 10.3748/wjg.v18.i28.3696

    Figure Lengend Snippet: Short hairpin RNA design, interference efficiency assay, and lentivirus transduction. A: DNA sequence analysis of pGCSIL/Interleukin-17A receptor (IL-17RA) short hairpin RNA (shRNA) 1; B: Lentiviral-mediated IL-17RA shRNA 1, 2, 3, and 4 (shRNA 1, 2, 3, and 4) inhibited IL-17RA mRNA expression in hepatic stellate cells (HSCs). HSCs infected with lentivirus at a multiplicity of infection of 10 for 72 h, and IL-17RA mRNA expression was quantified by polymerase chain reaction. IL-17RA shRNA 1 was the most efficient silencing tool for IL-17RA. b P

    Article Snippet: Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ).

    Techniques: shRNA, Transduction, Sequencing, Expressing, Infection, Polymerase Chain Reaction

    Mitogen activated protein kinases pathway involved in interleukin 17A induced interleukin 6 expression. A: Secretion of interleukin (IL)-6 in hepatic stellate cells (HSCs) induced by interleukin 17A (IL-17A) was determined using enzyme-linked immunosorbent assay. b P

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    doi: 10.3748/wjg.v18.i28.3696

    Figure Lengend Snippet: Mitogen activated protein kinases pathway involved in interleukin 17A induced interleukin 6 expression. A: Secretion of interleukin (IL)-6 in hepatic stellate cells (HSCs) induced by interleukin 17A (IL-17A) was determined using enzyme-linked immunosorbent assay. b P

    Article Snippet: Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay

    Lentiviral-mediated interleukin 17A receptor short hairpin RNA arrested interleukin 6 expression, partly through suppressing phosphorylation of p38 mitogen activated protein kinases and extracellular regulated protein kinases 1/2. A: Lentiviral-mediated interleukin (IL)-17A receptor short hairpin RNA (shRNA) 1 [at multiplicity of infection (MOI) = 10 for 72 h] inhibited the expression of IL-17RA in hepatic stellate cells (HSCs); B: Lentiviral-mediated IL-17RA shRNA 1 inhibited IL-17A-induced IL-6 mRNA expression in HSCs. HSCs were infected with IL-17RA shRNA 1 or random shRNA lentivirus at MOI = 10 for 72 h, and followed by 3 h exposure to IL-17A (100 ng/mL). b P

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    doi: 10.3748/wjg.v18.i28.3696

    Figure Lengend Snippet: Lentiviral-mediated interleukin 17A receptor short hairpin RNA arrested interleukin 6 expression, partly through suppressing phosphorylation of p38 mitogen activated protein kinases and extracellular regulated protein kinases 1/2. A: Lentiviral-mediated interleukin (IL)-17A receptor short hairpin RNA (shRNA) 1 [at multiplicity of infection (MOI) = 10 for 72 h] inhibited the expression of IL-17RA in hepatic stellate cells (HSCs); B: Lentiviral-mediated IL-17RA shRNA 1 inhibited IL-17A-induced IL-6 mRNA expression in HSCs. HSCs were infected with IL-17RA shRNA 1 or random shRNA lentivirus at MOI = 10 for 72 h, and followed by 3 h exposure to IL-17A (100 ng/mL). b P

    Article Snippet: Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ).

    Techniques: shRNA, Expressing, Infection