angiotensin iii  (Alomone Labs)


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    Structured Review

    Alomone Labs angiotensin iii
    ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist <t>Losartan</t> (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p
    Angiotensin Iii, 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
    https://www.bioz.com/result/angiotensin iii/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    angiotensin iii - by Bioz Stars, 2022-12
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    1) Product Images from "Sniffer cells for the detection of neural Angiotensin II in vitro"

    Article Title: Sniffer cells for the detection of neural Angiotensin II in vitro

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-45262-4

    ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG III induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p
    Figure Legend Snippet: ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG III induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p

    Techniques Used: Fluorescence, Transfection

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    Alomone Labs anti angiotensin ii receptor type 2 extracellular atto fluor 488 antibody
    Anti Angiotensin Ii Receptor Type 2 Extracellular Atto Fluor 488 Antibody, 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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    anti angiotensin ii receptor type 2 extracellular atto fluor 488 antibody - by Bioz Stars, 2022-12
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    93
    Alomone Labs anti angiotensin ii receptor type 1 extracellular antibody
    Expression of AT1-R and AT2-R in the peri-implantation endometrium. Representative micrographs of immunohistochemical stain of (a) AT1-R in fertile control, (b) AT1-R in RM, (c) AT2-R in fertile control, (d) AT2-R in RM. Magnification ×200. Scale bar = 200 μm. AT1-R, angiotensin type 1 receptor; AT2-R, angiotensin type 2 receptor; BV, blood vessels; GE, glandular epithelium; LE, luminal epithelium; RM, recurrent miscarriage; ST, stroma.
    Anti Angiotensin Ii Receptor Type 1 Extracellular Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Price from $9.99 to $1999.99
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    Expression of AT1-R and AT2-R in the peri-implantation endometrium. Representative micrographs of immunohistochemical stain of (a) AT1-R in fertile control, (b) AT1-R in RM, (c) AT2-R in fertile control, (d) AT2-R in RM. Magnification ×200. Scale bar = 200 μm. AT1-R, angiotensin type 1 receptor; AT2-R, angiotensin type 2 receptor; BV, blood vessels; GE, glandular epithelium; LE, luminal epithelium; RM, recurrent miscarriage; ST, stroma.

    Journal: Therapeutic Advances in Endocrinology and Metabolism

    Article Title: The role of the renin–angiotensin system in regulating endometrial neovascularization during the peri-implantation period: literature review and preliminary data

    doi: 10.1177/2042018820920560

    Figure Lengend Snippet: Expression of AT1-R and AT2-R in the peri-implantation endometrium. Representative micrographs of immunohistochemical stain of (a) AT1-R in fertile control, (b) AT1-R in RM, (c) AT2-R in fertile control, (d) AT2-R in RM. Magnification ×200. Scale bar = 200 μm. AT1-R, angiotensin type 1 receptor; AT2-R, angiotensin type 2 receptor; BV, blood vessels; GE, glandular epithelium; LE, luminal epithelium; RM, recurrent miscarriage; ST, stroma.

    Article Snippet: The primary antibodies were rabbit anti-human angiotensin II receptor type-1 polyclonal antibody (AAR-011, Alomone Labs, Jerusalem, Israel) at a dilution of 1:100 and rabbit anti-human angiotensin II type 2 receptor antibody (ab19134, AbCam, UK) at a dilution of 1:100.

    Techniques: Expressing, Immunohistochemistry, Staining

    The possible pathways of Ang II-mediated angiogenesis. ANG II stimulates the generation of ROS through membrane NAD(P)H oxidases in VSMCs after binding to AT1-R. ROS are involved in many Ang II mediated effects, including production of HIF-1α in vascular cells, activation of p38MAPK, and transcription factor NF-kB. Interactions between Ang II and ROS are critical in vascular physiology and pathology in terms of regulating vascular structure and functions. Ang-Tie could also trigger the production of ROS through NADPH oxidase. Ang II, angiotensin II; Ang-Tie, angiopoietin-Tie; AT1-R, angiotensin II type 1 (AT1) receptor; HIF-1α, hypoxia inducible factor-1α; NF-kB, nuclear factor kappa AB; ROS, reactive oxygen species; VSMCs, vascular smooth muscle cells.

    Journal: Therapeutic Advances in Endocrinology and Metabolism

    Article Title: The role of the renin–angiotensin system in regulating endometrial neovascularization during the peri-implantation period: literature review and preliminary data

    doi: 10.1177/2042018820920560

    Figure Lengend Snippet: The possible pathways of Ang II-mediated angiogenesis. ANG II stimulates the generation of ROS through membrane NAD(P)H oxidases in VSMCs after binding to AT1-R. ROS are involved in many Ang II mediated effects, including production of HIF-1α in vascular cells, activation of p38MAPK, and transcription factor NF-kB. Interactions between Ang II and ROS are critical in vascular physiology and pathology in terms of regulating vascular structure and functions. Ang-Tie could also trigger the production of ROS through NADPH oxidase. Ang II, angiotensin II; Ang-Tie, angiopoietin-Tie; AT1-R, angiotensin II type 1 (AT1) receptor; HIF-1α, hypoxia inducible factor-1α; NF-kB, nuclear factor kappa AB; ROS, reactive oxygen species; VSMCs, vascular smooth muscle cells.

    Article Snippet: The primary antibodies were rabbit anti-human angiotensin II receptor type-1 polyclonal antibody (AAR-011, Alomone Labs, Jerusalem, Israel) at a dilution of 1:100 and rabbit anti-human angiotensin II type 2 receptor antibody (ab19134, AbCam, UK) at a dilution of 1:100.

    Techniques: Binding Assay, Activation Assay

    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