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rhil 17a (R&D Systems)

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R&D Systems rhil 17a
Rhil 17a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 135 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+il+17a+rhil+17a/Recombinant+Human+IL-17A+Protein%2C+CF/pm40176290-126-22-23
Average 95 stars, based on 135 article reviews

rhil 17a - by Bioz Stars, 2026-09

95/100 stars

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Incubation:

Article Title: IL-17A Promotes RANTES Expression, But Not IL-16, in Orbital Fibroblasts Via CD40-CD40L Combination in Thyroid-Associated Ophthalmopathy.
Article Snippet: .. When reaching 70% confluence, cells were incubated in Dulbecco’s modified Eagle’s medium containing 1% fetal bovine serum for 16 hours before stimulation with recombinant human IL-17A (rhIL-17A) (1 ng/mL, 10 ng/mL, 20 ng/mL, 40 ng/mL, 100 ng/mL; R&D Systems, Minneapolis, MN, USA) in the presence or absence of rhCD40L (50 ng/mL; R&D Systems) for different time points; 0 ng/mL rhIL-17A served as a negative control. ..

Modification:

Recombinant:

Article Title: Effect of High, Medium, and Low Molecular Weight Hyaluronan on Inflammation and Oxidative Stress in an In Vitro Model of Human Nasal Epithelial Cells
Article Snippet: .. RPMI 2650 cells were stimulated with recombinant human IL-17A (rhIL-17A) (R&D Systems, Minneapolis, MN) (20 ng/mL) as previously described [ ]. .. To determine the role of the MAPK pathways in the activation of oxidative stress and IL-8 production, RPMI 2650 cells were stimulated with rhIL-17A for 30 min, 6 hrs, or 18 hrs in the presence or absence of inhibitor U0126 (1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenylmercapto) butadiene monoethanolate) (25 μ M) (Sigma-Aldrich s.r.l., Milan, Italy) (specific inhibitor of MEK1 and MEK2 MAP kinase kinase; MAPKK).

Negative Control:

Image Search Results

Human NPCs express IL17RA and respond to exogenous IL-17a by modulating the activity of ERK1/2 and mTORC1 signaling pathways. (A) Relative transcript levels of IL17RA in iPSC-derived NPCs of control ( n = 4) and ASD ( n = 7) subjects. (B) Relative protein levels of IL17RA in iPSC-derived NPCs of control ( n = 5) and ASD ( n = 7) subjects. β-actin was used as a loading control and representative immunoblot images are shown. Human NPCs endogenously express IL17RA. (C) Relative protein levels of IL17RA in iPSC-derived NPCs of control ( n = 2–3) and ASD ( n = 5) subjects after treatment with either vehicle (–) or rhIL-17a (10 and 50 ng/ml) for 48 h. The data are expressed as fold change in IL17RA expression relative to vehicle-treated samples. β-actin was used as a loading control and representative immunoblot images are shown. No significant differences in the protein levels of IL17RA were observed between rhIL-17a-treated and untreated human NPCs. (D) Time course analysis of pERK1/2 expression in iPSC-derived NPCs of control ( n = 4) and ASD ( n = 6) subjects after treatment with either vehicle (–) or rhIL-17a (50 ng/ml). Total-ERK was used as a loading control and the data are expressed as fold change in normalized pERK1/2 expression relative to vehicle-treated samples. Representative immunoblot images are shown. (E) Time course analysis of pRPS6 expression in iPSC-derived NPCs of control ( n = 3) and ASD ( n = 4) subjects after treatment with either vehicle (–) or rhIL-17a (50 ng/ml). β-actin was used as a loading control and the data are expressed as fold change in normalized pRPS6 expression relative to vehicle-treated. Representative immunoblot images are shown. Exogenous IL-17a led to a significant increase in pERK1/2 levels and significant decrease in pRPS6 levels in human NPCs. * p ≤ 0.05, ** p ≤ 0.01, and **** p ≤ 0.0001. (F) Time course analysis of pNF-kB65 expression in iPSC-derived astrocytes (used as positive control of pNF-kB expression) and in iPSC-derived NPCs of control ( n = 2) and ASD ( n = 1) subjects after treatment with either vehicle (–) or rhIL-17a (50 ng/ml). Total-NF-kB and β-actin were used as a loading controls and representative immunoblot images are shown. While iPSC-derived astrocytes express pNF-kB65, no detectable expression of this protein was observed in human NPCs.

Journal: Frontiers in Neuroscience

Article Title: Interleukin-17a Induces Neuronal Differentiation of Induced-Pluripotent Stem Cell-Derived Neural Progenitors From Autistic and Control Subjects

doi: 10.3389/fnins.2022.828646

Figure Lengend Snippet: Human NPCs express IL17RA and respond to exogenous IL-17a by modulating the activity of ERK1/2 and mTORC1 signaling pathways. (A) Relative transcript levels of IL17RA in iPSC-derived NPCs of control ( n = 4) and ASD ( n = 7) subjects. (B) Relative protein levels of IL17RA in iPSC-derived NPCs of control ( n = 5) and ASD ( n = 7) subjects. β-actin was used as a loading control and representative immunoblot images are shown. Human NPCs endogenously express IL17RA. (C) Relative protein levels of IL17RA in iPSC-derived NPCs of control ( n = 2–3) and ASD ( n = 5) subjects after treatment with either vehicle (–) or rhIL-17a (10 and 50 ng/ml) for 48 h. The data are expressed as fold change in IL17RA expression relative to vehicle-treated samples. β-actin was used as a loading control and representative immunoblot images are shown. No significant differences in the protein levels of IL17RA were observed between rhIL-17a-treated and untreated human NPCs. (D) Time course analysis of pERK1/2 expression in iPSC-derived NPCs of control ( n = 4) and ASD ( n = 6) subjects after treatment with either vehicle (–) or rhIL-17a (50 ng/ml). Total-ERK was used as a loading control and the data are expressed as fold change in normalized pERK1/2 expression relative to vehicle-treated samples. Representative immunoblot images are shown. (E) Time course analysis of pRPS6 expression in iPSC-derived NPCs of control ( n = 3) and ASD ( n = 4) subjects after treatment with either vehicle (–) or rhIL-17a (50 ng/ml). β-actin was used as a loading control and the data are expressed as fold change in normalized pRPS6 expression relative to vehicle-treated. Representative immunoblot images are shown. Exogenous IL-17a led to a significant increase in pERK1/2 levels and significant decrease in pRPS6 levels in human NPCs. * p ≤ 0.05, ** p ≤ 0.01, and **** p ≤ 0.0001. (F) Time course analysis of pNF-kB65 expression in iPSC-derived astrocytes (used as positive control of pNF-kB expression) and in iPSC-derived NPCs of control ( n = 2) and ASD ( n = 1) subjects after treatment with either vehicle (–) or rhIL-17a (50 ng/ml). Total-NF-kB and β-actin were used as a loading controls and representative immunoblot images are shown. While iPSC-derived astrocytes express pNF-kB65, no detectable expression of this protein was observed in human NPCs.

Article Snippet: To investigate whether treatment of NPCs with IL-17a could alter the expression of IL17RA, NPC samples were seeded in 60 mm plates at a density of 1 × 10 6 cells and were cultured in NPC medium containing either vehicle (ultrapure water) or human recombinant IL-17a (rhIL-17a) (Thermo Fischer Scientific) at 10 and 50 ng/ml for 48 h. The dosage of rhIL-17a and length of treatment were based on previous in vitro studies in mouse models examining the effect of exogenous IL-17a treatment on NPCs , astrocytes , and oligodendrocytes ( ; ).

Techniques: Activity Assay, Protein-Protein interactions, Derivative Assay, Control, Western Blot, Expressing, Positive Control

Exogenous IL-17a does not affect the proliferation and migration of human NPCs. (A) Line graph showing cell proliferation curves of iPSC-derived NPCs of control ( n = 5) and ASD ( n = 6) subjects cultured in the presence of either vehicle or rhIL-17a (10 and 50 ng/ml) for 24 and 48 h. (B) Line graph showing cell proliferation curves of iPSC-derived NPCs of control ( n = 5) and ASD ( n = 6) subjects cultured in the presence of either vehicle, or rhIL-17a (10 and 50 ng/ml), or rapamycin (5 nM, used as control), or rhIL-17a (50 ng/ml) plus rapamycin (5 nM) for 72 and 144 h. While rapamycin-treated human NPCs showed significantly decreased proliferation, ** p ≤ 0.01, no significant differences were observed in the proliferation rates between rhIL-17a-treated and untreated human NPCs. (C) Line graph of mean% relative wound density over time in iPSC-derived NPCs of control ( n = 5) and ASD ( n = 3) subjects cultured in the presence of either vehicle or rhIL-17a (10 and 50 ng/ml) for 24 h. No significant differences were observed in the migration rates between rhIL-17a-treated and untreated human NPCs.

Journal: Frontiers in Neuroscience

Article Title: Interleukin-17a Induces Neuronal Differentiation of Induced-Pluripotent Stem Cell-Derived Neural Progenitors From Autistic and Control Subjects

doi: 10.3389/fnins.2022.828646

Figure Lengend Snippet: Exogenous IL-17a does not affect the proliferation and migration of human NPCs. (A) Line graph showing cell proliferation curves of iPSC-derived NPCs of control ( n = 5) and ASD ( n = 6) subjects cultured in the presence of either vehicle or rhIL-17a (10 and 50 ng/ml) for 24 and 48 h. (B) Line graph showing cell proliferation curves of iPSC-derived NPCs of control ( n = 5) and ASD ( n = 6) subjects cultured in the presence of either vehicle, or rhIL-17a (10 and 50 ng/ml), or rapamycin (5 nM, used as control), or rhIL-17a (50 ng/ml) plus rapamycin (5 nM) for 72 and 144 h. While rapamycin-treated human NPCs showed significantly decreased proliferation, ** p ≤ 0.01, no significant differences were observed in the proliferation rates between rhIL-17a-treated and untreated human NPCs. (C) Line graph of mean% relative wound density over time in iPSC-derived NPCs of control ( n = 5) and ASD ( n = 3) subjects cultured in the presence of either vehicle or rhIL-17a (10 and 50 ng/ml) for 24 h. No significant differences were observed in the migration rates between rhIL-17a-treated and untreated human NPCs.

Techniques: Migration, Derivative Assay, Control, Cell Culture

Exogenous IL-17a stimulates neuronal differentiation of human NPCs. (A,B) Representative images (20× objective) of qualitative immunocytochemistry staining of iPSC-derived neurons of control and ASD subjects differentiated in the presence of either vehicle or rhIL-17a (10 or 50 ng/ml) for either 14 or 21 day showing the expression of the synaptic protein Synapsin-1 and the cytoskeleton protein MAP2. Nuclei were stained with DAPI (blue). Control- and ASD-derived neurons show characteristic neuronal morphology, and no gross differences were observed between the control and ASD groups. (C) Relative protein levels of markers for NPCs (SOX2 and Nestin), neurons (Synaptophysin-1, Synapsin-1, TUJ1, Homer-1 and MAP2) and astrocytes (GFAP) in iPSC-derived neurons of control ( n = 3–4) and ASD ( n = 3–6) subjects differentiated in the presence of either vehicle (–) or rhIL-17a (10 ng/ml) for 14 day. β-actin was used as a loading control and the data are expressed as fold change in normalized protein expression relative to vehicle-treated samples. Representative immunoblot images are shown. (D) Relative protein levels of markers for NPCs (SOX2), neurons (Synapsin-1, TUJ1, and MAP2) and astrocytes (GFAP) in iPSC-derived neurons of control ( n = 3–5) and ASD ( n = 3) subjects differentiated in the presence of either vehicle (–) or rhIL-17a (50 ng/ml) for 21 day. β-actin was used as a loading control and the data are expressed as fold change in normalized protein expression relative to vehicle-treated samples. Representative immunoblot images are shown. While no significant differences were found in the expression levels of NPC and astrocyte markers between rhIL-17a-treated and untreated cells, significantly increased levels of several neuron markers were observed in rhIL-17a-treated human NPCs. ** p ≤ 0.01, *** p ≤ 0.001.

Journal: Frontiers in Neuroscience

Article Title: Interleukin-17a Induces Neuronal Differentiation of Induced-Pluripotent Stem Cell-Derived Neural Progenitors From Autistic and Control Subjects

doi: 10.3389/fnins.2022.828646

Figure Lengend Snippet: Exogenous IL-17a stimulates neuronal differentiation of human NPCs. (A,B) Representative images (20× objective) of qualitative immunocytochemistry staining of iPSC-derived neurons of control and ASD subjects differentiated in the presence of either vehicle or rhIL-17a (10 or 50 ng/ml) for either 14 or 21 day showing the expression of the synaptic protein Synapsin-1 and the cytoskeleton protein MAP2. Nuclei were stained with DAPI (blue). Control- and ASD-derived neurons show characteristic neuronal morphology, and no gross differences were observed between the control and ASD groups. (C) Relative protein levels of markers for NPCs (SOX2 and Nestin), neurons (Synaptophysin-1, Synapsin-1, TUJ1, Homer-1 and MAP2) and astrocytes (GFAP) in iPSC-derived neurons of control ( n = 3–4) and ASD ( n = 3–6) subjects differentiated in the presence of either vehicle (–) or rhIL-17a (10 ng/ml) for 14 day. β-actin was used as a loading control and the data are expressed as fold change in normalized protein expression relative to vehicle-treated samples. Representative immunoblot images are shown. (D) Relative protein levels of markers for NPCs (SOX2), neurons (Synapsin-1, TUJ1, and MAP2) and astrocytes (GFAP) in iPSC-derived neurons of control ( n = 3–5) and ASD ( n = 3) subjects differentiated in the presence of either vehicle (–) or rhIL-17a (50 ng/ml) for 21 day. β-actin was used as a loading control and the data are expressed as fold change in normalized protein expression relative to vehicle-treated samples. Representative immunoblot images are shown. While no significant differences were found in the expression levels of NPC and astrocyte markers between rhIL-17a-treated and untreated cells, significantly increased levels of several neuron markers were observed in rhIL-17a-treated human NPCs. ** p ≤ 0.01, *** p ≤ 0.001.

Techniques: Immunocytochemistry, Staining, Derivative Assay, Control, Expressing, Western Blot

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