angiotensin ii  (Alomone Labs)


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    Alomone Labs angiotensin ii
    Angiotensin Ii, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 91 stars, based on 2 article reviews
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    Alomone Labs at1r
    <t>AT1R-dependent</t> ERK-phosphorylation after photolysis of [Tyr(DMNB) 4 ]Ang-II
    At1r, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Alomone Labs aar 012
    Angiotensin II AT 2 receptor immunocytochemistry in the mouse brain. (A) and (B) Antibody 2818-1 from Epitomics (dilution 1:400). The AT 2 receptor antibody reacts with parenchymal microvessels (indicated with arrowheads in A and B, and in box in panel A) in the cerebral motor cortex from -1.22 mm to Bregma, and the immunocytochemistry is similar in wild-type (WT) (A) and AT 2 knock-out (KO) mice (B). (C) and (D) Antibody sc-9040 from Santa Cruz (dilution 1:2000). The antibody detects ciliated ependymal cells (arrowheads) of the lateral ventricle (V), and the staining is similar in the wild type (C) or knockout mice (D) located at the same coordinates as A and B. (E) and (F): antibody <t>AAR-012</t> from Alomone (dilution 1:3000). In the cerebral motor cortex, the antibody detects cell colocalization with the neuronal marker NeuN (indicated with arrowheads in E and F and in the boxes in panel E). The staining is similar in wild-type (E) and AT 2 receptor knockout (F) mice. Scale bar = 20 µm.
    Aar 012, supplied by Alomone Labs, 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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    93
    Alomone Labs anti angiotensin ii receptor type 1 extracellular antibody
    Effects of sRAGE on Ang <t>II-induced</t> endothelial hyperpermeability in vivo. Twelve-week-old ApoE KO mice were used to investigate endothelial hyperpermeability. <t>Ang</t> <t>II</t> was injected into mice with or without sRAGE for 6 weeks. Then, Evans blue (EB) dye in saline was administered via the jugular vein. a Representative photographs of aortas stained with Evans blue in ApoE KO mice. b Quantification of positive areas of Evans blue staining in the aortas, as estimated using ImageJ. c Evans blue dye was eluted from the aortas by incubation with formamide. The amount of dye was quantified by spectrophotometry at 610 nm. d Representative TEM images of the EC junction area (original magnification, ×30,000). EL elastic lamina, EC endothelial cell; scale bar, 1000 nm. Control group, n = 10; Ang II group, n = 13; Ang II + sRAGE group, n = 11; sRAGE group, n = 7. The results are representative of at least four separate experiments. The values are presented as the means ± SEMs. * p
    Anti Angiotensin Ii Receptor Type 1 Extracellular Antibody, 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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    Price from $9.99 to $1999.99
    anti angiotensin ii receptor type 1 extracellular antibody - by Bioz Stars, 2022-09
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    AT1R-dependent ERK-phosphorylation after photolysis of [Tyr(DMNB) 4 ]Ang-II

    Journal: The Journal of Physiology

    Article Title: Photoreleasable ligands to study intracrine angiotensin II signalling

    doi: 10.1113/jphysiol.2014.279109

    Figure Lengend Snippet: AT1R-dependent ERK-phosphorylation after photolysis of [Tyr(DMNB) 4 ]Ang-II

    Article Snippet: By contrast, the caged analogues displaced [125 I]Ang-II with much higher IC50 values, indicating affinity reductions of 2–3 orders of magnitude: for AT1R and AT2R, respectively: [Tyr(DMNB)4 ]Ang-II, 1.1 μ m and 1.6 μ m ; Ang-II-ODMNB, 0.91 μ m and 0.47 μ m ; [Tyr(DMNB)4 ]Ang-II-ODMNB, 1.1 μ m and 1.9 μ m (Table ).

    Techniques:

    Angiotensin II AT 2 receptor immunocytochemistry in the mouse brain. (A) and (B) Antibody 2818-1 from Epitomics (dilution 1:400). The AT 2 receptor antibody reacts with parenchymal microvessels (indicated with arrowheads in A and B, and in box in panel A) in the cerebral motor cortex from -1.22 mm to Bregma, and the immunocytochemistry is similar in wild-type (WT) (A) and AT 2 knock-out (KO) mice (B). (C) and (D) Antibody sc-9040 from Santa Cruz (dilution 1:2000). The antibody detects ciliated ependymal cells (arrowheads) of the lateral ventricle (V), and the staining is similar in the wild type (C) or knockout mice (D) located at the same coordinates as A and B. (E) and (F): antibody AAR-012 from Alomone (dilution 1:3000). In the cerebral motor cortex, the antibody detects cell colocalization with the neuronal marker NeuN (indicated with arrowheads in E and F and in the boxes in panel E). The staining is similar in wild-type (E) and AT 2 receptor knockout (F) mice. Scale bar = 20 µm.

    Journal: PLoS ONE

    Article Title: Commercially Available Angiotensin II At2 Receptor Antibodies Are Nonspecific

    doi: 10.1371/journal.pone.0069234

    Figure Lengend Snippet: Angiotensin II AT 2 receptor immunocytochemistry in the mouse brain. (A) and (B) Antibody 2818-1 from Epitomics (dilution 1:400). The AT 2 receptor antibody reacts with parenchymal microvessels (indicated with arrowheads in A and B, and in box in panel A) in the cerebral motor cortex from -1.22 mm to Bregma, and the immunocytochemistry is similar in wild-type (WT) (A) and AT 2 knock-out (KO) mice (B). (C) and (D) Antibody sc-9040 from Santa Cruz (dilution 1:2000). The antibody detects ciliated ependymal cells (arrowheads) of the lateral ventricle (V), and the staining is similar in the wild type (C) or knockout mice (D) located at the same coordinates as A and B. (E) and (F): antibody AAR-012 from Alomone (dilution 1:3000). In the cerebral motor cortex, the antibody detects cell colocalization with the neuronal marker NeuN (indicated with arrowheads in E and F and in the boxes in panel E). The staining is similar in wild-type (E) and AT 2 receptor knockout (F) mice. Scale bar = 20 µm.

    Article Snippet: The antibody dilutions were as follows: sc-9040, 1:500; AAR-012, 1:200; 2818-1, 1:1000, as recommended by the manufacturers.

    Techniques: Immunocytochemistry, Knock-Out, Mouse Assay, Staining, Marker

    Effects of sRAGE on Ang II-induced endothelial hyperpermeability in vivo. Twelve-week-old ApoE KO mice were used to investigate endothelial hyperpermeability. Ang II was injected into mice with or without sRAGE for 6 weeks. Then, Evans blue (EB) dye in saline was administered via the jugular vein. a Representative photographs of aortas stained with Evans blue in ApoE KO mice. b Quantification of positive areas of Evans blue staining in the aortas, as estimated using ImageJ. c Evans blue dye was eluted from the aortas by incubation with formamide. The amount of dye was quantified by spectrophotometry at 610 nm. d Representative TEM images of the EC junction area (original magnification, ×30,000). EL elastic lamina, EC endothelial cell; scale bar, 1000 nm. Control group, n = 10; Ang II group, n = 13; Ang II + sRAGE group, n = 11; sRAGE group, n = 7. The results are representative of at least four separate experiments. The values are presented as the means ± SEMs. * p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: Effects of sRAGE on Ang II-induced endothelial hyperpermeability in vivo. Twelve-week-old ApoE KO mice were used to investigate endothelial hyperpermeability. Ang II was injected into mice with or without sRAGE for 6 weeks. Then, Evans blue (EB) dye in saline was administered via the jugular vein. a Representative photographs of aortas stained with Evans blue in ApoE KO mice. b Quantification of positive areas of Evans blue staining in the aortas, as estimated using ImageJ. c Evans blue dye was eluted from the aortas by incubation with formamide. The amount of dye was quantified by spectrophotometry at 610 nm. d Representative TEM images of the EC junction area (original magnification, ×30,000). EL elastic lamina, EC endothelial cell; scale bar, 1000 nm. Control group, n = 10; Ang II group, n = 13; Ang II + sRAGE group, n = 11; sRAGE group, n = 7. The results are representative of at least four separate experiments. The values are presented as the means ± SEMs. * p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: In Vivo, Mouse Assay, Injection, Staining, Incubation, Spectrophotometry, Transmission Electron Microscopy

    Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin. a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin. a As Ang II binds to and stimulates AT1R, the expression and secretion of HMGB1 can be increased by NF-κB activation. NF-κB-mediated expression of proinflammatory molecules, including RAGE itself, can occur. HMGB1 binds to RAGE, which can induce RAGE-mediated activation of Src/β-catenin/VE-cadherin via mDia1. b Blockade of RAGE activation by sRAGE attenuates the Ang II-induced increase in endothelial hyperpermeability by inhibiting RAGE-mediated signaling pathways

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Transduction, Expressing, Activation Assay

    Importance of the AT1R-RAGE axis in Ang II-induced endothelial hyperpermeability in HUVECs. a Changes in the phosphorylation of VE-cadherin (Y731), Src (Tyr416), and β-catenin (Ser552) in HUVECs following transfection with RAGE siRNA and treatment with Ang II. Expression values were normalized to those of VE-cadherin, Src, and β-catenin ( n = 4 for each lane). b Immunocytochemistry of VE-cadherin (green) and DAPI (nuclei, blue), as examined under a confocal microscope (white scale bars: 50 μm in merged images and 20 μm in magnified images; ×400 magnification). The main images were selected from representative regions. c HUVECs transfected with siRNA targeting RAGE or with scrambled sequences were incubated for 72 h and were then stimulated with Ang II for 6 h. TEER was measured every 2 h. *** p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: Importance of the AT1R-RAGE axis in Ang II-induced endothelial hyperpermeability in HUVECs. a Changes in the phosphorylation of VE-cadherin (Y731), Src (Tyr416), and β-catenin (Ser552) in HUVECs following transfection with RAGE siRNA and treatment with Ang II. Expression values were normalized to those of VE-cadherin, Src, and β-catenin ( n = 4 for each lane). b Immunocytochemistry of VE-cadherin (green) and DAPI (nuclei, blue), as examined under a confocal microscope (white scale bars: 50 μm in merged images and 20 μm in magnified images; ×400 magnification). The main images were selected from representative regions. c HUVECs transfected with siRNA targeting RAGE or with scrambled sequences were incubated for 72 h and were then stimulated with Ang II for 6 h. TEER was measured every 2 h. *** p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Transfection, Expressing, Immunocytochemistry, Microscopy, Incubation

    HMGB1 is an important mediator of AT1R-RAGE signaling. HUVECs were treated with Ang II in the absence or presence of losartan for 4 h. a HMGB1 release in supernatants was measured by ELISA and western blotting ( n = 4 for each lane). b , c HUVECs were incubated with Ang II in the presence or absence of anti-HMGB1-neutralizing antibody (50 ng/ml) for 4 h and analyzed by western blotting. The relative values of AT1R, RAGE, and mDia1 expression were normalized to that of GAPDH ( n = 4 for each lane). The relative values of phospho-VE-cadherin expression were normalized to that of VE-cadherin ( n = 3 for each lane). The values are presented as the means ± SEMs. * p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: HMGB1 is an important mediator of AT1R-RAGE signaling. HUVECs were treated with Ang II in the absence or presence of losartan for 4 h. a HMGB1 release in supernatants was measured by ELISA and western blotting ( n = 4 for each lane). b , c HUVECs were incubated with Ang II in the presence or absence of anti-HMGB1-neutralizing antibody (50 ng/ml) for 4 h and analyzed by western blotting. The relative values of AT1R, RAGE, and mDia1 expression were normalized to that of GAPDH ( n = 4 for each lane). The relative values of phospho-VE-cadherin expression were normalized to that of VE-cadherin ( n = 3 for each lane). The values are presented as the means ± SEMs. * p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Incubation, Expressing

    Soluble RAGE (sRAGE) attenuates Ang II-induced endothelial hyperpermeability. a HUVECs were treated with sRAGE (2 μg/ml) for 1 h and were then subjected to Ang II treatment for 4 h. Endothelial permeability was assessed in media from the lower chambers after the addition of FITC-dextran 40 to the upper chambers for 1 h ( n = 3 for each lane). b TEER was measured every 2 h. * p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: Soluble RAGE (sRAGE) attenuates Ang II-induced endothelial hyperpermeability. a HUVECs were treated with sRAGE (2 μg/ml) for 1 h and were then subjected to Ang II treatment for 4 h. Endothelial permeability was assessed in media from the lower chambers after the addition of FITC-dextran 40 to the upper chambers for 1 h ( n = 3 for each lane). b TEER was measured every 2 h. * p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Permeability

    RAGE regulates Ang II-induced endothelial hyperpermeability via mDia1. a HUVECs were transfected with mDia1 siRNA and cultured in the presence of Ang II for an additional 4 h. Western blot analysis was performed to observe changes in phospho-Src, phospho-β-catenin, and phospho-VE-cadherin protein expression ( n = 4 for each lane). b Changes in mDia1 protein levels in HUVECs following transfection with RAGE siRNA, as determined by western blotting. Expression was normalized to that of GAPDH ( n = 3 for each lane). c Changes in mDia1 mRNA expression in HUVECs following transfection with RAGE siRNA, as determined by RT-PCR. Expression was normalized to that of the 18S rRNA gene ( n = 4 for each lane). d HUVECs were treated with Ang II and the NF-κB inhibitor (5 μg/ml) alone or in combination for 4 h. Protein levels of AT1R, RAGE, and mDia1 in cell lysates were determined by western blotting. Expression was normalized to that of GAPDH ( n = 4 for each lane). The values are presented as the means ± SEMs. * p

    Journal: Experimental & Molecular Medicine

    Article Title: Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE

    doi: 10.1038/s12276-019-0312-5

    Figure Lengend Snippet: RAGE regulates Ang II-induced endothelial hyperpermeability via mDia1. a HUVECs were transfected with mDia1 siRNA and cultured in the presence of Ang II for an additional 4 h. Western blot analysis was performed to observe changes in phospho-Src, phospho-β-catenin, and phospho-VE-cadherin protein expression ( n = 4 for each lane). b Changes in mDia1 protein levels in HUVECs following transfection with RAGE siRNA, as determined by western blotting. Expression was normalized to that of GAPDH ( n = 3 for each lane). c Changes in mDia1 mRNA expression in HUVECs following transfection with RAGE siRNA, as determined by RT-PCR. Expression was normalized to that of the 18S rRNA gene ( n = 4 for each lane). d HUVECs were treated with Ang II and the NF-κB inhibitor (5 μg/ml) alone or in combination for 4 h. Protein levels of AT1R, RAGE, and mDia1 in cell lysates were determined by western blotting. Expression was normalized to that of GAPDH ( n = 4 for each lane). The values are presented as the means ± SEMs. * p

    Article Snippet: Anti-AT1R antibody (AAR-011) was purchased from Alomone Labs (Hadassah Ein Kerem, Israel).

    Techniques: Transfection, Cell Culture, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction

    Loss of Cx37 selectively alters the expression of some Ang II ‐stimulated signals. The levels of transcripts coding for Angiotensinogen (Agt), Angiotensin receptor 1a (Agtr1a), and Angiotensin receptor 1b (Agtr1b) were similar in the aortas of WT and Cx37−/− mice. In contrast, the transcripts coding for Angiotensin receptor 2 (Agtr2), Connector enhancer of kinase suppressor of Ras 1 (Cnksr1), SH 2 domain‐containing tyrosine phosphatase 2 (Ptpn6), and Glutamyl aminopeptidase A (Enpep), which all contribute to control the Ang II pathway, were increased in the aortas of Cx37−/− mice. N=9. Results are means+ SEM . * P ≤0.05, *** P ≤0.001 vs WT mice, as given by t test. Ang II indicates angiotensin II ; Cx37, Connexin37; WT , wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension

    doi: 10.1161/JAHA.118.010823

    Figure Lengend Snippet: Loss of Cx37 selectively alters the expression of some Ang II ‐stimulated signals. The levels of transcripts coding for Angiotensinogen (Agt), Angiotensin receptor 1a (Agtr1a), and Angiotensin receptor 1b (Agtr1b) were similar in the aortas of WT and Cx37−/− mice. In contrast, the transcripts coding for Angiotensin receptor 2 (Agtr2), Connector enhancer of kinase suppressor of Ras 1 (Cnksr1), SH 2 domain‐containing tyrosine phosphatase 2 (Ptpn6), and Glutamyl aminopeptidase A (Enpep), which all contribute to control the Ang II pathway, were increased in the aortas of Cx37−/− mice. N=9. Results are means+ SEM . * P ≤0.05, *** P ≤0.001 vs WT mice, as given by t test. Ang II indicates angiotensin II ; Cx37, Connexin37; WT , wild type.

    Article Snippet: The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500).

    Techniques: Expressing, Mouse Assay

    Cx37−/− mice become rapidly normotensive after the 2K1C procedure. A , One month after the 2K1C surgery, WT mice were significantly hypertensive, compared with their sham‐operated controls, whereas Cx37−/− mice featured a control SBP (systolic blood pressure). WT sham (sham‐operated controls) N=15; Cx37−/− sham N=14; WT 2K1C (2‐kidney, 1‐clip) N=19; Cx37−/− 2K1C N=17. B , Compared with controls infused with NaCl, both WT and Cx37−/− mice showed a significant increase in SBP after a daily infusion of 0.25 mg Ang II /kg body weight during 1 month. However, this increase was significantly lower in Cx37−/− than in WT mice. WT NaCl, Cx37−/− NaCl N=7; WT Ang II (angiotensin II ); Cx37−/− Ang II N=8. C , In contrast, the mice of these 2 genotypes showed a similar increase in blood pressure, after a daily treatment with l ‐ NAME ( N ‐nitro‐ l ‐arginine‐methyl‐ester, 500 mg/L in the drinking water) for 1 month. N=6. Results are means+ SEM . * P ≤0.05 and *** P ≤0.001 vs respective control mice; °°° P ≤0.001 vs WT mice, as given by 2‐way ANOVA . Ang II indicates angiotensin II; Cx37, connexin37; n.s., not significant; WT , wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension

    doi: 10.1161/JAHA.118.010823

    Figure Lengend Snippet: Cx37−/− mice become rapidly normotensive after the 2K1C procedure. A , One month after the 2K1C surgery, WT mice were significantly hypertensive, compared with their sham‐operated controls, whereas Cx37−/− mice featured a control SBP (systolic blood pressure). WT sham (sham‐operated controls) N=15; Cx37−/− sham N=14; WT 2K1C (2‐kidney, 1‐clip) N=19; Cx37−/− 2K1C N=17. B , Compared with controls infused with NaCl, both WT and Cx37−/− mice showed a significant increase in SBP after a daily infusion of 0.25 mg Ang II /kg body weight during 1 month. However, this increase was significantly lower in Cx37−/− than in WT mice. WT NaCl, Cx37−/− NaCl N=7; WT Ang II (angiotensin II ); Cx37−/− Ang II N=8. C , In contrast, the mice of these 2 genotypes showed a similar increase in blood pressure, after a daily treatment with l ‐ NAME ( N ‐nitro‐ l ‐arginine‐methyl‐ester, 500 mg/L in the drinking water) for 1 month. N=6. Results are means+ SEM . * P ≤0.05 and *** P ≤0.001 vs respective control mice; °°° P ≤0.001 vs WT mice, as given by 2‐way ANOVA . Ang II indicates angiotensin II; Cx37, connexin37; n.s., not significant; WT , wild type.

    Article Snippet: The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500).

    Techniques: Mouse Assay, Cross-linking Immunoprecipitation

    Loss of Cx37−/− alters the increase in blood pressure in models of renin‐dependent hypertension. A , WT mice receiving daily 1 mg Ang II /kg body weight displayed a 50% increase in systolic blood pressure ( SBP ). Under the same conditions, Cx37−/− mice displayed a significantly lower increase of SBP . WT NaCl N=5; Cx37−/− NaCl, WT Ang II (angiotensin II ), Cx37−/− Ang II N=6. B , Similar observations were made in mice receiving daily 0.25 mg Ang II /kg body weight WT NaCl, Cx37−/− NaCl N=7; WT Ang II , Cx37−/− Ang II N=8. C , Two weeks after the 2K1C (2‐kidney, 1‐clip) procedure, Cx37−/− mice also showed a lower increase in SBP than WT controls. WT sham (sham‐operated controls) WT 2K1C, N=5; Cx37−/− sham, Cx37−/− 2K1C N=6. D , In contrast, both types of mice became similarly hypertensive after a treatment with l ‐ NAME ( N ‐nitro‐ l ‐arginine‐methyl‐ester); N=6. *** P ≤0.001 vs corresponding controls (NaCl‐infused or sham‐operated animals); °°° P ≤0.001 vs WT mice, as given by 2‐way ANOVA of AUC (areas under the SBP curve). Ang II indicates angiotensin II; Cx37, connexin37; WT , wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension

    doi: 10.1161/JAHA.118.010823

    Figure Lengend Snippet: Loss of Cx37−/− alters the increase in blood pressure in models of renin‐dependent hypertension. A , WT mice receiving daily 1 mg Ang II /kg body weight displayed a 50% increase in systolic blood pressure ( SBP ). Under the same conditions, Cx37−/− mice displayed a significantly lower increase of SBP . WT NaCl N=5; Cx37−/− NaCl, WT Ang II (angiotensin II ), Cx37−/− Ang II N=6. B , Similar observations were made in mice receiving daily 0.25 mg Ang II /kg body weight WT NaCl, Cx37−/− NaCl N=7; WT Ang II , Cx37−/− Ang II N=8. C , Two weeks after the 2K1C (2‐kidney, 1‐clip) procedure, Cx37−/− mice also showed a lower increase in SBP than WT controls. WT sham (sham‐operated controls) WT 2K1C, N=5; Cx37−/− sham, Cx37−/− 2K1C N=6. D , In contrast, both types of mice became similarly hypertensive after a treatment with l ‐ NAME ( N ‐nitro‐ l ‐arginine‐methyl‐ester); N=6. *** P ≤0.001 vs corresponding controls (NaCl‐infused or sham‐operated animals); °°° P ≤0.001 vs WT mice, as given by 2‐way ANOVA of AUC (areas under the SBP curve). Ang II indicates angiotensin II; Cx37, connexin37; WT , wild type.

    Article Snippet: The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500).

    Techniques: Mouse Assay, Cross-linking Immunoprecipitation

    Loss of Cx37 selectively alters the expression of the AT 2 receptors in the aortas of Cx37−/− mice. A , Immunofluorescence showed a similar staining for AT 1R (upper panels) in the aortas of all WT and Cx37−/− mice. In contrast, the staining for AT 2R was more intense in the aortas of Cx37−/− than in WT mice. Bar=20 μm. L indicates lumen; M, media. B , Western blot showed that the aortas of WT and Cx37−/− mice expressed similar levels of the AT 1R protein. C , In contrast, the basal levels of the AT 2R protein were higher in Cx37−/− than in WT mice, and were not increased after the 2K1C surgery. WT sham N=21; Cx37−/− sham N=17; WT 2K1C N=19; Cx37−/− 2K1C N=17. D and E , Comparable observations were made for both AT 1R ( D ) and AT 2R ( E ) in mice infused daily with 1 mg Ang II /kg body weight WT NaCl N=4; Cx37−/− NaCl, Cx37−/− Ang II N=3, WT Ang II N=6. Results are means+ SEM . ° P ≤0.05 vs WT mice, as given by 2‐way ANOVA . 2K1C indicates 2‐kidney, 1‐clip; Ang II , angiotensin II ; AT 1R, Ang II type 1 receptors; AT 2R, Ang II type 2 receptors; Cx37, Connexin37; DAPI, 4′,6‐diamidino‐2‐phenylindole; Sham, sham‐operated controls; WT , wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension

    doi: 10.1161/JAHA.118.010823

    Figure Lengend Snippet: Loss of Cx37 selectively alters the expression of the AT 2 receptors in the aortas of Cx37−/− mice. A , Immunofluorescence showed a similar staining for AT 1R (upper panels) in the aortas of all WT and Cx37−/− mice. In contrast, the staining for AT 2R was more intense in the aortas of Cx37−/− than in WT mice. Bar=20 μm. L indicates lumen; M, media. B , Western blot showed that the aortas of WT and Cx37−/− mice expressed similar levels of the AT 1R protein. C , In contrast, the basal levels of the AT 2R protein were higher in Cx37−/− than in WT mice, and were not increased after the 2K1C surgery. WT sham N=21; Cx37−/− sham N=17; WT 2K1C N=19; Cx37−/− 2K1C N=17. D and E , Comparable observations were made for both AT 1R ( D ) and AT 2R ( E ) in mice infused daily with 1 mg Ang II /kg body weight WT NaCl N=4; Cx37−/− NaCl, Cx37−/− Ang II N=3, WT Ang II N=6. Results are means+ SEM . ° P ≤0.05 vs WT mice, as given by 2‐way ANOVA . 2K1C indicates 2‐kidney, 1‐clip; Ang II , angiotensin II ; AT 1R, Ang II type 1 receptors; AT 2R, Ang II type 2 receptors; Cx37, Connexin37; DAPI, 4′,6‐diamidino‐2‐phenylindole; Sham, sham‐operated controls; WT , wild type.

    Article Snippet: The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500).

    Techniques: Expressing, Mouse Assay, Immunofluorescence, Staining, Western Blot, Cross-linking Immunoprecipitation

    Loss of Cx37 does not alter the expression of several signals involved in the Ang II effects. The levels of transcripts coding for the chymase (Cma1), which converts Ang I to Ang II , the Regulator of G‐protein signaling 2 (Rgs2), which negatively regulates AT 1R function by modulating its Gαq subunit activity, the Dual specificity protein phosphatase 1 (Dusp1), an AT 2R‐associated phosphatase that contributes to AT 2R‐mediated inactivation of the ERK cascade, and Mas1, the receptor for Ang‐(1–7) that promotes vasodilatation, were similar in the aortas of WT and Cx37−/− mice. WT N=9; Cx37−/− N=8. Results are means+ SEM . Statistical analysis was performed using t test. Ang indicates angiotensin; AT 1R, Ang II type 1 receptors; AT 2R, Ang II type 2 receptors; Cx37, Connexin37; WT , wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension

    doi: 10.1161/JAHA.118.010823

    Figure Lengend Snippet: Loss of Cx37 does not alter the expression of several signals involved in the Ang II effects. The levels of transcripts coding for the chymase (Cma1), which converts Ang I to Ang II , the Regulator of G‐protein signaling 2 (Rgs2), which negatively regulates AT 1R function by modulating its Gαq subunit activity, the Dual specificity protein phosphatase 1 (Dusp1), an AT 2R‐associated phosphatase that contributes to AT 2R‐mediated inactivation of the ERK cascade, and Mas1, the receptor for Ang‐(1–7) that promotes vasodilatation, were similar in the aortas of WT and Cx37−/− mice. WT N=9; Cx37−/− N=8. Results are means+ SEM . Statistical analysis was performed using t test. Ang indicates angiotensin; AT 1R, Ang II type 1 receptors; AT 2R, Ang II type 2 receptors; Cx37, Connexin37; WT , wild type.

    Article Snippet: The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500).

    Techniques: Expressing, Activity Assay, Mouse Assay

    Loss of Cx37−/− alters the activation of downstream key signaling proteins to the Ang II signaling pathway. A through C , After a 2‐hour exposure to 40 μmol/L Ang II , the levels of phosphorylated ERK ( A ), MLC 2 ( B ), and AKT ( C ) increased in the aortas of WT but not of Cx37−/− mice. WT Ctl, WT Ang II N=3; Cx37−/− Ctl, Cx37−/− Ang II N=5. Results are means+ SEM . * P ≤0.05 vs respective control mice and ° P ≤0.05, °° P ≤0.01 vs WT mice, as given by 2‐way ANOVA . Ang II indicates angiotensin II ; Ctl, control; Cx37, Connexin37; MLC 2, myosin light chain 2; WT , wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Connexin37‐Dependent Mechanisms Selectively Contribute to Modulate Angiotensin II‐Mediated Hypertension

    doi: 10.1161/JAHA.118.010823

    Figure Lengend Snippet: Loss of Cx37−/− alters the activation of downstream key signaling proteins to the Ang II signaling pathway. A through C , After a 2‐hour exposure to 40 μmol/L Ang II , the levels of phosphorylated ERK ( A ), MLC 2 ( B ), and AKT ( C ) increased in the aortas of WT but not of Cx37−/− mice. WT Ctl, WT Ang II N=3; Cx37−/− Ctl, Cx37−/− Ang II N=5. Results are means+ SEM . * P ≤0.05 vs respective control mice and ° P ≤0.05, °° P ≤0.01 vs WT mice, as given by 2‐way ANOVA . Ang II indicates angiotensin II ; Ctl, control; Cx37, Connexin37; MLC 2, myosin light chain 2; WT , wild type.

    Article Snippet: The membranes were then incubated overnight at 4°C with 1 of the following primary antibodies: rabbit polyclonal antibodies against AT1R (Alomone labs, AAR‐011, 1:1000), AT2R (Alomone labs, AAR‐012, 1:1000), MLC2 (Cell Signaling, 3672, 1:1000), P‐MLC2 (Cell Signaling, 3674, 1:1000), ERK (Cell Signaling, 4695, 1:1000), P‐ERK (Cell Signaling, 9101, 1:1000), AKT (Cell Signaling, 9272S, 1:1000), Cx40 (Chemicon, AB1726; 1:250), Cx37 (Biotrend Chemikalien, Cx37A11‐A; 1:500), Cx43 (Cell Signaling, 3512S, 1:500) or Cx45 (Millipore, AB1745, 1:500); mouse monoclonal antibodies against eNOS (BD Biosciences, 610297, 1:500), PeNOS (BD Biosciences, 612392, 1:500), P‐AKT (Cell Signaling, 4051, 1:500), and α‐tubulin (Sigma‐Aldrich, T5168; 1:2500).

    Techniques: Activation Assay, Mouse Assay