b1r  (Alomone Labs)


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    Alomone Labs b1r
    Effect of <t>B1R</t> activation on ADAM17 activity in primary hypothalamic neurons. ( A ) Incubation of wild-type neurons with B1R-specific agonist Lys-Des-Arg 9 -Bradykinin (LDABK) significantly increased ADAM17 activity. Pre-treatment with R715, a B1R-specific antagonist, prevented this LDABK-mediated increase in ADAM17 activity. R715 treatment alone did not have any effect on ADAM17 activity. ( B ) Treatment with LDABK did not show any effect on ADAM17 activity in neurons with B1R deletion. In addition, the HOE 140, a kinin B2 receptor (B2R)-specific antagonist also did not show any effect on ADAM17 activity. The cultured primary neurons were pre-treated with a specific B1R antagonist (R715, 10 μM) or a specific B2R antagonist HOE 140 (HOE, 10 μM) for 1 h, followed by treatment with LDABK (300 nM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p
    B1r, 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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    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    b1r - by Bioz Stars, 2022-01
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    1) Product Images from "Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons"

    Article Title: Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22010145

    Effect of B1R activation on ADAM17 activity in primary hypothalamic neurons. ( A ) Incubation of wild-type neurons with B1R-specific agonist Lys-Des-Arg 9 -Bradykinin (LDABK) significantly increased ADAM17 activity. Pre-treatment with R715, a B1R-specific antagonist, prevented this LDABK-mediated increase in ADAM17 activity. R715 treatment alone did not have any effect on ADAM17 activity. ( B ) Treatment with LDABK did not show any effect on ADAM17 activity in neurons with B1R deletion. In addition, the HOE 140, a kinin B2 receptor (B2R)-specific antagonist also did not show any effect on ADAM17 activity. The cultured primary neurons were pre-treated with a specific B1R antagonist (R715, 10 μM) or a specific B2R antagonist HOE 140 (HOE, 10 μM) for 1 h, followed by treatment with LDABK (300 nM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Effect of B1R activation on ADAM17 activity in primary hypothalamic neurons. ( A ) Incubation of wild-type neurons with B1R-specific agonist Lys-Des-Arg 9 -Bradykinin (LDABK) significantly increased ADAM17 activity. Pre-treatment with R715, a B1R-specific antagonist, prevented this LDABK-mediated increase in ADAM17 activity. R715 treatment alone did not have any effect on ADAM17 activity. ( B ) Treatment with LDABK did not show any effect on ADAM17 activity in neurons with B1R deletion. In addition, the HOE 140, a kinin B2 receptor (B2R)-specific antagonist also did not show any effect on ADAM17 activity. The cultured primary neurons were pre-treated with a specific B1R antagonist (R715, 10 μM) or a specific B2R antagonist HOE 140 (HOE, 10 μM) for 1 h, followed by treatment with LDABK (300 nM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Activation Assay, Activity Assay, Incubation, Cell Culture

    Effect of B1R activation on ACE2 activity in primary hypothalamic neurons. ( A ) Incubation of wild-type neurons with B1R-specific agonist LDABK significantly decreased ACE2 activity. R715, a B1R-specific antagonist pretreatment prevented this LDABK-mediated decrease in ACE2 activity. R715 treatment alone did not have any effect on ACE2 activity. ( B ) Treatment with LDABK did not show any effect on ACE2 activity in neurons with B1R deletion. In addition, the HOE 140, a B2R-specific antagonist also did not show any effect on ACE2 activity. The cultured primary neurons were pre-treated with a specific B1R antagonist (R715, 10 μM) or a specific B2R antagonist HOE 140 (HOE, 10 μM) for 1 h, followed by treatment with LDABK (300 nM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Effect of B1R activation on ACE2 activity in primary hypothalamic neurons. ( A ) Incubation of wild-type neurons with B1R-specific agonist LDABK significantly decreased ACE2 activity. R715, a B1R-specific antagonist pretreatment prevented this LDABK-mediated decrease in ACE2 activity. R715 treatment alone did not have any effect on ACE2 activity. ( B ) Treatment with LDABK did not show any effect on ACE2 activity in neurons with B1R deletion. In addition, the HOE 140, a B2R-specific antagonist also did not show any effect on ACE2 activity. The cultured primary neurons were pre-treated with a specific B1R antagonist (R715, 10 μM) or a specific B2R antagonist HOE 140 (HOE, 10 μM) for 1 h, followed by treatment with LDABK (300 nM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Activation Assay, Activity Assay, Incubation, Cell Culture

    Effect of glutamate on B1R activation in primary hypothalamic neurons. Representative triple immunostaining revealed that compared to vehicle ( A ) treatment, stimulation with glutamate (100 μM) ( B ) for 18 h induced the expression of kinin B1R and ADAM17 protein in primary hypothalamic neurons. This glutamate-induced increase in B1R and ADAM17 protein expression was prevented by pre-treatment with R715 ( C ). Treatment with glutamate (100 μM) for 4 h induced an increase in B1R mRNA in cultured neurons, measured by real time PCR. This increase in B1R mRNA was prevented by pre-treatment with R715 ( D ). Representative image of Western blot ( E ) and quantitative analysis ( F ) showing glutamate stimulation induced B1R protein expression which was prevented by pre-treatment with R715 in neurons ( n = 4–6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Effect of glutamate on B1R activation in primary hypothalamic neurons. Representative triple immunostaining revealed that compared to vehicle ( A ) treatment, stimulation with glutamate (100 μM) ( B ) for 18 h induced the expression of kinin B1R and ADAM17 protein in primary hypothalamic neurons. This glutamate-induced increase in B1R and ADAM17 protein expression was prevented by pre-treatment with R715 ( C ). Treatment with glutamate (100 μM) for 4 h induced an increase in B1R mRNA in cultured neurons, measured by real time PCR. This increase in B1R mRNA was prevented by pre-treatment with R715 ( D ). Representative image of Western blot ( E ) and quantitative analysis ( F ) showing glutamate stimulation induced B1R protein expression which was prevented by pre-treatment with R715 in neurons ( n = 4–6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Activation Assay, Triple Immunostaining, Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Western Blot

    Kinin B1 receptor (B1R), A Disintegrin And Metalloprotease 17 (ADAM17), and angiotensin converting enzyme 2 (ACE2) expression in primary hypothalamic neurons. Representative photomicrographs showing immunofluorescence staining for neuron-specific marker microtubule associated protein 2 (MAP-2) (Green) in primary neurons from wild-type ( A ) and B1R knockout mice ( B ) cultured for 10 days. Primary neurons from wild-type mice pups showed immunopositivity for the presence of B1R ( C ), while B1R immunoreactivity was absent in neurons with B1R deletion ( D ). Representative triple immunostaining revealed that kinin B1R ( E ) and ADAM17 ( F ) are expressed in primary hypothalamic neurons expressing nuclear DAPI staining in blue ( G ), and merged image ( H ) shows the colocalization of B1R and ADAM17. Representative triple immunostaining showing ACE2 and ADAM17 expression and co-localization in wild-type neurons ( I – L ) and in B1R knockout neurons ( M – P ).
    Figure Legend Snippet: Kinin B1 receptor (B1R), A Disintegrin And Metalloprotease 17 (ADAM17), and angiotensin converting enzyme 2 (ACE2) expression in primary hypothalamic neurons. Representative photomicrographs showing immunofluorescence staining for neuron-specific marker microtubule associated protein 2 (MAP-2) (Green) in primary neurons from wild-type ( A ) and B1R knockout mice ( B ) cultured for 10 days. Primary neurons from wild-type mice pups showed immunopositivity for the presence of B1R ( C ), while B1R immunoreactivity was absent in neurons with B1R deletion ( D ). Representative triple immunostaining revealed that kinin B1R ( E ) and ADAM17 ( F ) are expressed in primary hypothalamic neurons expressing nuclear DAPI staining in blue ( G ), and merged image ( H ) shows the colocalization of B1R and ADAM17. Representative triple immunostaining showing ACE2 and ADAM17 expression and co-localization in wild-type neurons ( I – L ) and in B1R knockout neurons ( M – P ).

    Techniques Used: Expressing, Immunofluorescence, Staining, Marker, Knock-Out, Mouse Assay, Cell Culture, Triple Immunostaining

    Activation of kinin B1R upregulates ADAM17-mediated ACE2 shedding in primary hypothalamic neurons. B1R activation by specific agonist results in upregulation of ADAM17 expression and activity which results in increased membrane-bound ACE2 shedding and reduced ACE2 activity in primary hypothalamic neurons. In addition, glutamate can induce B1R expression and B1R is involved in glutamate-mediated effects on ADAM17 activity and ACE2 shedding.
    Figure Legend Snippet: Activation of kinin B1R upregulates ADAM17-mediated ACE2 shedding in primary hypothalamic neurons. B1R activation by specific agonist results in upregulation of ADAM17 expression and activity which results in increased membrane-bound ACE2 shedding and reduced ACE2 activity in primary hypothalamic neurons. In addition, glutamate can induce B1R expression and B1R is involved in glutamate-mediated effects on ADAM17 activity and ACE2 shedding.

    Techniques Used: Activation Assay, Expressing, Activity Assay

    Glutamate-induced ADAM17-mediated ACE2 shedding involves kinin B1R activation. Glutamate increased ADAM17 activity ( A ) and decreased ACE2 activity ( B ) in neurons, which was prevented by pre-treatment with R715. Treatment of B1R knockout neurons with glutamate did not show any effect on ADAM17 or ACE2 activity. ADAM17 and ACE2 assays were performed in primary hypothalamic neurons cultured from wild-type and B1R knockout neonates, treated with glutamate (Glut, 100 μM) or glutamate with 1 h of pre-treatment with R715 (a specific B1R inhibitor, 10 μM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Glutamate-induced ADAM17-mediated ACE2 shedding involves kinin B1R activation. Glutamate increased ADAM17 activity ( A ) and decreased ACE2 activity ( B ) in neurons, which was prevented by pre-treatment with R715. Treatment of B1R knockout neurons with glutamate did not show any effect on ADAM17 or ACE2 activity. ADAM17 and ACE2 assays were performed in primary hypothalamic neurons cultured from wild-type and B1R knockout neonates, treated with glutamate (Glut, 100 μM) or glutamate with 1 h of pre-treatment with R715 (a specific B1R inhibitor, 10 μM) for 18 h ( n = 6 independent cultures/group). Statistical significance: one-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Activation Assay, Activity Assay, Knock-Out, Cell Culture

    2) Product Images from "Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons"

    Article Title: Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons

    Journal: Cellular and molecular neurobiology

    doi: 10.1007/s10571-019-00778-1

    B1R antagonist treatment reduced angiotensin II induced NF-κB binding activity in primary hypothalamic neurons. The cultured primary neurons are pre-treated with B1R specific antagonist (R715, 10 μM) for 1 hour, followed by treatment with vehicle or angiotensin II (Ang II, 300 nM) for 24 hours. NF-kB DNA binding activity was analyzed by NF-kB p65 transcription factor assay kit. The result of NF-kB DNA binding showed that Ang II treatment significant increased NF-kB p65 DNA binding activity in primary neurons, and treatment with R715 significantly attenuated this effect. (n=6 independent culture wells/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: B1R antagonist treatment reduced angiotensin II induced NF-κB binding activity in primary hypothalamic neurons. The cultured primary neurons are pre-treated with B1R specific antagonist (R715, 10 μM) for 1 hour, followed by treatment with vehicle or angiotensin II (Ang II, 300 nM) for 24 hours. NF-kB DNA binding activity was analyzed by NF-kB p65 transcription factor assay kit. The result of NF-kB DNA binding showed that Ang II treatment significant increased NF-kB p65 DNA binding activity in primary neurons, and treatment with R715 significantly attenuated this effect. (n=6 independent culture wells/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Binding Assay, Activity Assay, Cell Culture, Transcription Factor Assay

    B1R antagonist treatment prevented angiotensin II-induced decrease in mitochondrial respiration in primary hypothalamic neurons. Primary hypothalamic mouse neurons were cultured on Seahorse XF-24 plates and treated with vehicle or Ang II with or without R715 for 24 hours. Seahorse mito stress assay was performed to measure oxygen consumption rate (OCR). (A). Bioenergetic profile following sequential injection of oligomycin ( O ), FCCP ( F ) and antimycin A/rotenone ( A/R ) indicating the key parameters of mitochondrial respiration in neurons. OCR measurements showed that Ang II stimulation resulted in significant decrease in basal respiration (B), ATP production (C), maximal respiration (D), and spare respiratory capacity (E) indicating mitochondrial dysfunction, and treatment with R715 prevented this Ang II-induced mitochondrial dysfunction. (n=8 independent culture wells/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: B1R antagonist treatment prevented angiotensin II-induced decrease in mitochondrial respiration in primary hypothalamic neurons. Primary hypothalamic mouse neurons were cultured on Seahorse XF-24 plates and treated with vehicle or Ang II with or without R715 for 24 hours. Seahorse mito stress assay was performed to measure oxygen consumption rate (OCR). (A). Bioenergetic profile following sequential injection of oligomycin ( O ), FCCP ( F ) and antimycin A/rotenone ( A/R ) indicating the key parameters of mitochondrial respiration in neurons. OCR measurements showed that Ang II stimulation resulted in significant decrease in basal respiration (B), ATP production (C), maximal respiration (D), and spare respiratory capacity (E) indicating mitochondrial dysfunction, and treatment with R715 prevented this Ang II-induced mitochondrial dysfunction. (n=8 independent culture wells/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Cell Culture, Injection

    Angiotensin II-induced neuroinflammation and oxidative stress are mediated by kinin B1R. Mouse neonatal primary hypothermic neurons express both B1R and AT1R. Ang II stimulation of neurons increased expression of B1R, which in turn increased resulted in upregulation of Nox2 and Nox4 expression, and NF-κB activation, and ultimately leading to expression of pro-inflammatory cytokine production. Treatment with R715, the specific B1R antagonist blunted angiotensin II-induced neuroinflammation and oxidative stress by reducing Nox gene expression and attenuating NF-κB activation.
    Figure Legend Snippet: Angiotensin II-induced neuroinflammation and oxidative stress are mediated by kinin B1R. Mouse neonatal primary hypothermic neurons express both B1R and AT1R. Ang II stimulation of neurons increased expression of B1R, which in turn increased resulted in upregulation of Nox2 and Nox4 expression, and NF-κB activation, and ultimately leading to expression of pro-inflammatory cytokine production. Treatment with R715, the specific B1R antagonist blunted angiotensin II-induced neuroinflammation and oxidative stress by reducing Nox gene expression and attenuating NF-κB activation.

    Techniques Used: Expressing, Activation Assay

    Angiotensin II-induced inflammatory gene expression is reduced by treatment with B1R antagonist in primary hypothalamic neurons. Angiotensin II treatment induced neuroinflammation as indicated by increase in pro-inflammatory genes (A) cyclooxygenase (Cox2), (B) Interleukin (IL)-1β, (C) IL-6, and (D) tumor necrosis factor (TNF). This increase in neuroinflammation was prevented by pre-treatment with R715. The cultured primary neurons are pre-treated with a specific B1R antagonist (R715, 10 μM) for 1 hour, followed by treatment with angiotensin II (Ang II, 300 nM) for 6 hours. The gene expression was measured using real time RT-PCR in triplicates. (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Angiotensin II-induced inflammatory gene expression is reduced by treatment with B1R antagonist in primary hypothalamic neurons. Angiotensin II treatment induced neuroinflammation as indicated by increase in pro-inflammatory genes (A) cyclooxygenase (Cox2), (B) Interleukin (IL)-1β, (C) IL-6, and (D) tumor necrosis factor (TNF). This increase in neuroinflammation was prevented by pre-treatment with R715. The cultured primary neurons are pre-treated with a specific B1R antagonist (R715, 10 μM) for 1 hour, followed by treatment with angiotensin II (Ang II, 300 nM) for 6 hours. The gene expression was measured using real time RT-PCR in triplicates. (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Expressing, Cell Culture, Quantitative RT-PCR

    Kinin B1 receptor gene expression is induced by angiotensin II in primary hypothalamic neurons. Brightfield photomicrograph showing primary mouse hypothalamic neuron cultures grown for 5 days (A). Representative photomicrographs showing immunofluorescence staining for neuron specific marker microtubule associated protein 2, MAP-2 (Red) and glial cell specific marker glial fibrillary acidic protein, GFAP (Green) in primary neurons cultured for 10 days without Ara-C (B) and with Ara-C (C) treatment. Treatment with Ara-C for 14 days resulted in primarily predominant neuronal population as stained for neuronal marker MAP-2 (D). Triple immunostaining revealed that Kinin B1R (E) and AT1R (F) are expressed in primary hypothalamic neurons. Treatment with angiotensin II (300 nM) induced increase in B1R mRNA levels in cultured neurons, measured by real time PCR (G). (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Kinin B1 receptor gene expression is induced by angiotensin II in primary hypothalamic neurons. Brightfield photomicrograph showing primary mouse hypothalamic neuron cultures grown for 5 days (A). Representative photomicrographs showing immunofluorescence staining for neuron specific marker microtubule associated protein 2, MAP-2 (Red) and glial cell specific marker glial fibrillary acidic protein, GFAP (Green) in primary neurons cultured for 10 days without Ara-C (B) and with Ara-C (C) treatment. Treatment with Ara-C for 14 days resulted in primarily predominant neuronal population as stained for neuronal marker MAP-2 (D). Triple immunostaining revealed that Kinin B1R (E) and AT1R (F) are expressed in primary hypothalamic neurons. Treatment with angiotensin II (300 nM) induced increase in B1R mRNA levels in cultured neurons, measured by real time PCR (G). (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Expressing, Immunofluorescence, Staining, Marker, Cell Culture, Acetylene Reduction Assay, Triple Immunostaining, Real-time Polymerase Chain Reaction

    B1R antagonist treatment reduced angiotensin II induced reactive oxygen species (ROS) production in primary hypothalamic neurons. (A). Representative photomicrographs showing dihydroethidium (DHE) stained primary hypothalamic neurons. (B). DHE staining quantified as corrected total cell fluorescence shows increased superoxide generation by treatment with angiotensin II (Ang II), which was attenuated by R715 treatment. (n=8/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: B1R antagonist treatment reduced angiotensin II induced reactive oxygen species (ROS) production in primary hypothalamic neurons. (A). Representative photomicrographs showing dihydroethidium (DHE) stained primary hypothalamic neurons. (B). DHE staining quantified as corrected total cell fluorescence shows increased superoxide generation by treatment with angiotensin II (Ang II), which was attenuated by R715 treatment. (n=8/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Staining, Fluorescence

    Angiotensin II-induced Nox2 and Nox4 gene expression was reduced by treatment with B1R antagonist in primary hypothalamic neurons. Angiotensin II treatment induced oxidative stress by increased gene expression of (A) Nox2 and (B) Nox4. This increase was attenuated or prevented by pre-treatment with R715. The cultured primary neurons are pre-treated with a specific B1R antagonist (R715, 10 μM) for 1 hour, followed by treatment with angiotensin II (Ang II, 300 nM) for 6 hours. The gene expression was measured using real time RT-PCR in triplicates. (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p
    Figure Legend Snippet: Angiotensin II-induced Nox2 and Nox4 gene expression was reduced by treatment with B1R antagonist in primary hypothalamic neurons. Angiotensin II treatment induced oxidative stress by increased gene expression of (A) Nox2 and (B) Nox4. This increase was attenuated or prevented by pre-treatment with R715. The cultured primary neurons are pre-treated with a specific B1R antagonist (R715, 10 μM) for 1 hour, followed by treatment with angiotensin II (Ang II, 300 nM) for 6 hours. The gene expression was measured using real time RT-PCR in triplicates. (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. * p

    Techniques Used: Expressing, Cell Culture, Quantitative RT-PCR

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    • anti at1r antibody  (Alomone Labs)
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    Schematic diagram of signal transduction pathways involved in Ang II-induced endothelial hyperpermeability via <t>AT1R/RAGE/mDia1/Src/β-catenin/VE-cadherin.</t> 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
    Anti At1r 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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    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

    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

    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

    Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a normal sodium diet (all n = 5).

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    Article Title: Sex differences in acute ANG II-mediated hemodynamic responses in mice

    doi: 10.1152/ajpregu.00638.2009

    Figure Lengend Snippet: Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a normal sodium diet (all n = 5).

    Article Snippet: All blots were incubated overnight with the following primary antibodies: anti-AT1 receptor (Alomone Labs, Jerusalem, Israel), anti-AT2 receptor antibody (Alomone Labs), and anti-endothelial nitric oxide synthase 3 (NOS3) (BD Biosciences, San Jose, CA).

    Techniques: Expressing, Mouse Assay

    Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ), in kidney vessels from male and female mice on a low-sodium diet (all n = 5).

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    Article Title: Sex differences in acute ANG II-mediated hemodynamic responses in mice

    doi: 10.1152/ajpregu.00638.2009

    Figure Lengend Snippet: Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ), in kidney vessels from male and female mice on a low-sodium diet (all n = 5).

    Article Snippet: All blots were incubated overnight with the following primary antibodies: anti-AT1 receptor (Alomone Labs, Jerusalem, Israel), anti-AT2 receptor antibody (Alomone Labs), and anti-endothelial nitric oxide synthase 3 (NOS3) (BD Biosciences, San Jose, CA).

    Techniques: Expressing, Mouse Assay

    Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a high-sodium diet (all n = 5).

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    Article Title: Sex differences in acute ANG II-mediated hemodynamic responses in mice

    doi: 10.1152/ajpregu.00638.2009

    Figure Lengend Snippet: Expression of the AT1 receptor ( A ), AT2 receptor ( B ), and NOS3 ( C ) in kidney vessels from male and female mice on a high-sodium diet (all n = 5).

    Article Snippet: All blots were incubated overnight with the following primary antibodies: anti-AT1 receptor (Alomone Labs, Jerusalem, Israel), anti-AT2 receptor antibody (Alomone Labs), and anti-endothelial nitric oxide synthase 3 (NOS3) (BD Biosciences, San Jose, CA).

    Techniques: Expressing, Mouse Assay

    Subcellular distribution of P2Y2, P2Y4, and P2Y6 receptors in MEFs. WT or KI MEFs were cultured and, after changing the medium, were maintained in the absence or presence of 1 μ M DFU for 2 h. Cells were fixed with paraformaldehyde (4%; pH 7.2) and permeabilized with cold methanol at RT. After incubation with anti-P2Y2, anti-P2Y4 and anti-P2Y6 antibodies (1 : 500) overnight at 4°C, cells were visualized by confocal microscopy using a FITC-conjugated secondary Ab (Alexa-Fluor 488, 1 : 1000). Nuclei were stained with Hoechst 33258. Coverslips were mounted in Prolong Gold antifade reagent (Molecular Probes) and the intensity of the fluorescence was measured using Image J software (NIH, Bethesda, MD, USA). Results show the mean + SD of three experiments. ** P

    Journal: Mediators of Inflammation

    Article Title: Sustained Release of Prostaglandin E2 in Fibroblasts Expressing Ectopically Cyclooxygenase 2 Impairs P2Y-Dependent Ca2+-Mobilization

    doi: 10.1155/2014/832103

    Figure Lengend Snippet: Subcellular distribution of P2Y2, P2Y4, and P2Y6 receptors in MEFs. WT or KI MEFs were cultured and, after changing the medium, were maintained in the absence or presence of 1 μ M DFU for 2 h. Cells were fixed with paraformaldehyde (4%; pH 7.2) and permeabilized with cold methanol at RT. After incubation with anti-P2Y2, anti-P2Y4 and anti-P2Y6 antibodies (1 : 500) overnight at 4°C, cells were visualized by confocal microscopy using a FITC-conjugated secondary Ab (Alexa-Fluor 488, 1 : 1000). Nuclei were stained with Hoechst 33258. Coverslips were mounted in Prolong Gold antifade reagent (Molecular Probes) and the intensity of the fluorescence was measured using Image J software (NIH, Bethesda, MD, USA). Results show the mean + SD of three experiments. ** P

    Article Snippet: Antibodies against P2Y2, P2Y4, and P2Y6 receptors were from Alomone Labs (Jerusalem, Israel) and other antibodies were from Santa Cruz Biotech (Santa Cruz, CA, USA), from Cell Signaling (Danvers, MA, USA), or from the sources previously described [ ].

    Techniques: Cell Culture, Incubation, Confocal Microscopy, Staining, Fluorescence, Software