rabbit anti-a2bar polyclonal antibody Search Results


93
Alomone Labs anti adenosine a2b receptor
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Anti Adenosine A2b Receptor, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Alomone Labs polyclonal rabbit anti human a2bar antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Polyclonal Rabbit Anti Human A2bar Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Alomone Labs adenosine a2b receptor (extracellular) blocking peptide
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Adenosine A2b Receptor (Extracellular) Blocking Peptide, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss cd16 polyclonal antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
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Bioss pge2 polyclonal antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Pge2 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss 8-ohdg polyclonal antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
8 Ohdg Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss cdc2/cdk1 polyclonal antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Cdc2/Cdk1 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Bioss bs-0021m
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Bs 0021m, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bioss prrsv m protein polyclonal antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
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Bioss collagen 7 polyclonal antibody
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
Collagen 7 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Becton Dickinson hif1α ab
CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine <t>A2b</t> receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .
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93
Biorbyt antibody against a2bar
Figure 2. Immunohistochemical analysis of glomerular alterations in diabetic rats. (A) The panels show representative immunofluorescent images of the detection of <t>A2BAR,</t> α-SMA, ZO-1, nephrin, and Snail in renal tissue from control rats, diabetic nephropathy (DN) rats, and diabetic rats treated with the A2BAR antagonist MRS1754 (DN + MRS1754). The images emphasize changes in the levels of these proteins within the glomerulus. Nuclear staining with DAPI is in blue. The bar indicates 50 µm. (B) The graphs correspond to the means ± SD of relative fluorescent units (RFUs) of a quantitative analysis of A2BAR, α-SMA, ZO-1, nephrin, and Snail in glomeruli from the control (white bar), diabetic (black bar), and MRS1754-treated diabetic (grey bar) rat groups. The means in the control group were normalized to 1. Images of 12 glomeruli from 2 control, 4 diabetic, and 4 treated diabetic rats were analyzed. *, p < 0.05 vs. control; #, p < 0.05 vs. diabetes.
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Image Search Results


CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine A2b receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .

Journal: Frontiers in Pharmacology

Article Title: BAY 60-6583 Enhances the Antitumor Function of Chimeric Antigen Receptor-Modified T Cells Independent of the Adenosine A2b Receptor

doi: 10.3389/fphar.2021.619800

Figure Lengend Snippet: CAR T cell enhancement by BAY 60-6583 in CD133 CAR T cells seems not to be dependent on the adenosine A2b receptor. (A, B) Blocking of the adenosine A2b receptor cannot inhibit the enhanced antitumor activities induced by BAY 60-6583. In the anti-CD133 CAR T co-culture system (E:T ratio of 4:1), the adenosine A2b receptor was blocked by 1 μM PSB603 1 h before 10 μM BAY 60-6583 or 1 μM NECA was added. 24 h later, TNF-α production (A) and tumor lysis (B) were analyzed (C) The expression of the adenosine A2b receptor on conventional (WT) and A2b receptor knockout (4 + 6) anti-CD133 CAR T cells was determined by Western blot. Data from a representative experiment of n = 4 experiments (D, E) BAY 60-6583-induced enhancement of CAR T cell-mediated antitumor activities were not influenced by adenosine A2b receptor deficiency. Conventional and A2b receptor knockout anti-CD133 CAR T cells were co-cultured with U251-CD133OE luc cells at an E:T ratio of 4:1. After treatment with vehicle control or BAY 60-6583 for 24 h, cytokine secretion in the supernatant was detected (D) ; 48 h later, cytotoxicity was assessed (E) . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by 1-way (A, B) or 2-way ANOVA (D, E) . Data are represented as the mean ± SD from a representative experiment of n = 3 experiments (A, B, D, E) .

Article Snippet: After blocking with 5% milk for 1 h, the membranes were incubated with anti-adenosine A2b receptor (AAR-003, alomone labs) or anti-GAPDH (sc-32233, Santa Cruz Biotechnology) antibodies at 4°C overnight.

Techniques: Blocking Assay, Co-Culture Assay, Lysis, Expressing, Knock-Out, Western Blot, Cell Culture, Control

Figure 2. Immunohistochemical analysis of glomerular alterations in diabetic rats. (A) The panels show representative immunofluorescent images of the detection of A2BAR, α-SMA, ZO-1, nephrin, and Snail in renal tissue from control rats, diabetic nephropathy (DN) rats, and diabetic rats treated with the A2BAR antagonist MRS1754 (DN + MRS1754). The images emphasize changes in the levels of these proteins within the glomerulus. Nuclear staining with DAPI is in blue. The bar indicates 50 µm. (B) The graphs correspond to the means ± SD of relative fluorescent units (RFUs) of a quantitative analysis of A2BAR, α-SMA, ZO-1, nephrin, and Snail in glomeruli from the control (white bar), diabetic (black bar), and MRS1754-treated diabetic (grey bar) rat groups. The means in the control group were normalized to 1. Images of 12 glomeruli from 2 control, 4 diabetic, and 4 treated diabetic rats were analyzed. *, p < 0.05 vs. control; #, p < 0.05 vs. diabetes.

Journal: Cells

Article Title: Adenosine A 2B Receptor Antagonism Interferes with TGF-β Cellular Signaling Through SMAD2/-3 and p65-Nf-κB in Podocytes and Protects from Phenotypical Transformation in Experimental Diabetic Glomerulopathy.

doi: 10.3390/cells14120890

Figure Lengend Snippet: Figure 2. Immunohistochemical analysis of glomerular alterations in diabetic rats. (A) The panels show representative immunofluorescent images of the detection of A2BAR, α-SMA, ZO-1, nephrin, and Snail in renal tissue from control rats, diabetic nephropathy (DN) rats, and diabetic rats treated with the A2BAR antagonist MRS1754 (DN + MRS1754). The images emphasize changes in the levels of these proteins within the glomerulus. Nuclear staining with DAPI is in blue. The bar indicates 50 µm. (B) The graphs correspond to the means ± SD of relative fluorescent units (RFUs) of a quantitative analysis of A2BAR, α-SMA, ZO-1, nephrin, and Snail in glomeruli from the control (white bar), diabetic (black bar), and MRS1754-treated diabetic (grey bar) rat groups. The means in the control group were normalized to 1. Images of 12 glomeruli from 2 control, 4 diabetic, and 4 treated diabetic rats were analyzed. *, p < 0.05 vs. control; #, p < 0.05 vs. diabetes.

Article Snippet: The samples were incubated with an antibody against A2BAR (dilution of 1:250, cat. orb234999, Biorbyt Ltd., Cambridge, UK), anti-α-SMA (dilution of 1:100, cat. sc-130617, Santa Cruz Biotech, Dallas, TX, USA), anti-ZO1 (dilution of 1:100, cat. 61-7300, Thermo Fisher Scientific, USA), anti-nephrin (dilution of 1:100, cat. PA5-106921, Thermo Fisher Scientific, USA), and anti-Snail (dilution of 1:100, cat. ab53519, Abcam, Cambridge, UK) overnight at 4 ◦C.

Techniques: Immunohistochemical staining, Control, Staining

Figure 3. A2BAR antagonism prevents the loss of podocyte epithelial markers in diabetic glomeru- lopathy. (A) Representative Western blot analysis showing the levels of epithelial ZO-1 and nephrin, as well as mesenchymal α-SMA and Snail, in purified glomeruli from the different rat groups. (B) The graphs represent the means and SD of the levels of epithelial and mesenchymal markers relative to β-actin. The means in the control group were normalized to 1. (C) Representative Western blot analysis of the Snail distribution in cell fractions purified from the kidneys of experimental rat groups. (D) The graph represents the ratio of the Snail subcellular distribution. The mean in the control was normalized to 1. The number of animals analyzed in each experimental group was 5 in (B) and 2 in (D). *, p < 0.05 vs. control; #, p < 0.05 vs. DN; &, p < 0.05 vs. control.

Journal: Cells

Article Title: Adenosine A 2B Receptor Antagonism Interferes with TGF-β Cellular Signaling Through SMAD2/-3 and p65-Nf-κB in Podocytes and Protects from Phenotypical Transformation in Experimental Diabetic Glomerulopathy.

doi: 10.3390/cells14120890

Figure Lengend Snippet: Figure 3. A2BAR antagonism prevents the loss of podocyte epithelial markers in diabetic glomeru- lopathy. (A) Representative Western blot analysis showing the levels of epithelial ZO-1 and nephrin, as well as mesenchymal α-SMA and Snail, in purified glomeruli from the different rat groups. (B) The graphs represent the means and SD of the levels of epithelial and mesenchymal markers relative to β-actin. The means in the control group were normalized to 1. (C) Representative Western blot analysis of the Snail distribution in cell fractions purified from the kidneys of experimental rat groups. (D) The graph represents the ratio of the Snail subcellular distribution. The mean in the control was normalized to 1. The number of animals analyzed in each experimental group was 5 in (B) and 2 in (D). *, p < 0.05 vs. control; #, p < 0.05 vs. DN; &, p < 0.05 vs. control.

Article Snippet: The samples were incubated with an antibody against A2BAR (dilution of 1:250, cat. orb234999, Biorbyt Ltd., Cambridge, UK), anti-α-SMA (dilution of 1:100, cat. sc-130617, Santa Cruz Biotech, Dallas, TX, USA), anti-ZO1 (dilution of 1:100, cat. 61-7300, Thermo Fisher Scientific, USA), anti-nephrin (dilution of 1:100, cat. PA5-106921, Thermo Fisher Scientific, USA), and anti-Snail (dilution of 1:100, cat. ab53519, Abcam, Cambridge, UK) overnight at 4 ◦C.

Techniques: Western Blot, Purification, Control