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  • 94
    Alomone Labs anti b1 bradykinin receptor bdkrb1 antibody
    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
    Anti B1 Bradykinin Receptor Bdkrb1 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
    https://www.bioz.com/result/anti b1 bradykinin receptor bdkrb1 antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti b1 bradykinin receptor bdkrb1 antibody - by Bioz Stars, 2022-10
    94/100 stars
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    80
    Abcam anti b1 bradykinin receptor bdkrb1 antibody
    <t>B1R</t> gene deletion prevents inflammation in the kidney during DOCA-salt-induced hypertension. DOCA-salt treatment for 3 weeks significantly increased mRNA expression of pro-inflammatory cytokines TNF, IL-6, IL-1β and chemokine MCP-1 in the kidney cortex of wild-type (WT) mice compared with sham mice. B1R knockout (B1RKO) mice did not show this DOCA-salt-induced increase in inflammatory markers. Gene expression measured by real time RT-PCR. Data was normalized to β-actin and presented as mean ± SEM ( n = 6, Two-way ANOVA, * P
    Anti B1 Bradykinin Receptor Bdkrb1 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti b1 bradykinin receptor bdkrb1 antibody/product/Abcam
    Average 80 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti b1 bradykinin receptor bdkrb1 antibody - by Bioz Stars, 2022-10
    80/100 stars
      Buy from Supplier

    Image Search Results


    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

    Journal: International Journal of Molecular Sciences

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

    doi: 10.3390/ijms22010145

    Figure Lengend 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

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of ADAM17 (#ab13535, lot GR56873-25, Abcam, Cambridge, UK, 1:500 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel, 1:200 dilution) or ACE2 ((#OASG00144, lot 1442701, Aviva systems biology, San Diego, CA, USA, 1:200 dilution) coupled with DAPI staining.

    Techniques: 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

    Journal: International Journal of Molecular Sciences

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

    doi: 10.3390/ijms22010145

    Figure Lengend 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

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of ADAM17 (#ab13535, lot GR56873-25, Abcam, Cambridge, UK, 1:500 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel, 1:200 dilution) or ACE2 ((#OASG00144, lot 1442701, Aviva systems biology, San Diego, CA, USA, 1:200 dilution) coupled with DAPI staining.

    Techniques: 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

    Journal: International Journal of Molecular Sciences

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

    doi: 10.3390/ijms22010145

    Figure Lengend 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

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of ADAM17 (#ab13535, lot GR56873-25, Abcam, Cambridge, UK, 1:500 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel, 1:200 dilution) or ACE2 ((#OASG00144, lot 1442701, Aviva systems biology, San Diego, CA, USA, 1:200 dilution) coupled with DAPI staining.

    Techniques: 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 ).

    Journal: International Journal of Molecular Sciences

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

    doi: 10.3390/ijms22010145

    Figure Lengend 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 ).

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of ADAM17 (#ab13535, lot GR56873-25, Abcam, Cambridge, UK, 1:500 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel, 1:200 dilution) or ACE2 ((#OASG00144, lot 1442701, Aviva systems biology, San Diego, CA, USA, 1:200 dilution) coupled with DAPI staining.

    Techniques: 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.

    Journal: International Journal of Molecular Sciences

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

    doi: 10.3390/ijms22010145

    Figure Lengend 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.

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of ADAM17 (#ab13535, lot GR56873-25, Abcam, Cambridge, UK, 1:500 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel, 1:200 dilution) or ACE2 ((#OASG00144, lot 1442701, Aviva systems biology, San Diego, CA, USA, 1:200 dilution) coupled with DAPI staining.

    Techniques: 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

    Journal: International Journal of Molecular Sciences

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

    doi: 10.3390/ijms22010145

    Figure Lengend 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

    Article Snippet: Triple immunostaining was performed with specific validated antibodies for detection of ADAM17 (#ab13535, lot GR56873-25, Abcam, Cambridge, UK, 1:500 dilution) and B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel, 1:200 dilution) or ACE2 ((#OASG00144, lot 1442701, Aviva systems biology, San Diego, CA, USA, 1:200 dilution) coupled with DAPI staining.

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

    B1R gene deletion prevents inflammation in the kidney during DOCA-salt-induced hypertension. DOCA-salt treatment for 3 weeks significantly increased mRNA expression of pro-inflammatory cytokines TNF, IL-6, IL-1β and chemokine MCP-1 in the kidney cortex of wild-type (WT) mice compared with sham mice. B1R knockout (B1RKO) mice did not show this DOCA-salt-induced increase in inflammatory markers. Gene expression measured by real time RT-PCR. Data was normalized to β-actin and presented as mean ± SEM ( n = 6, Two-way ANOVA, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R gene deletion prevents inflammation in the kidney during DOCA-salt-induced hypertension. DOCA-salt treatment for 3 weeks significantly increased mRNA expression of pro-inflammatory cytokines TNF, IL-6, IL-1β and chemokine MCP-1 in the kidney cortex of wild-type (WT) mice compared with sham mice. B1R knockout (B1RKO) mice did not show this DOCA-salt-induced increase in inflammatory markers. Gene expression measured by real time RT-PCR. Data was normalized to β-actin and presented as mean ± SEM ( n = 6, Two-way ANOVA, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Expressing, Mouse Assay, Knock-Out, Quantitative RT-PCR

    B1R expression is increased and correlates with collagen expression in human kidney sections from hypertensive chronic kidney disease. Representative immunohistochemistry photomicrographs showing B1R specific immunoreactivity in kidney sections of healthy controls (A) , specifically in glomerulus (B) , tubules (C) and arteries (D) . The B1R specific immunoreactivity is increased in kidney sections from renal disease (E) , specifically in glomerulus (F) , tubules (G) and arteries (H) . Representative photomicrographs showing Masson Trichrome staining for collagen deposition in health control kidney section (I) with in glomerulus (J) , tubules (K) and arteries (L) . The collagen deposition was increased in kidney sections from the kidney disease subjects (M) , specifically in glomerulus (N) , tubules (O) and arteries (P) . Quantification data showing increased B1R (Q) and collagen (R) expression in kidney sections from renal disease subjects ( n = 5, Unpaired, 2-tailed t -test, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R expression is increased and correlates with collagen expression in human kidney sections from hypertensive chronic kidney disease. Representative immunohistochemistry photomicrographs showing B1R specific immunoreactivity in kidney sections of healthy controls (A) , specifically in glomerulus (B) , tubules (C) and arteries (D) . The B1R specific immunoreactivity is increased in kidney sections from renal disease (E) , specifically in glomerulus (F) , tubules (G) and arteries (H) . Representative photomicrographs showing Masson Trichrome staining for collagen deposition in health control kidney section (I) with in glomerulus (J) , tubules (K) and arteries (L) . The collagen deposition was increased in kidney sections from the kidney disease subjects (M) , specifically in glomerulus (N) , tubules (O) and arteries (P) . Quantification data showing increased B1R (Q) and collagen (R) expression in kidney sections from renal disease subjects ( n = 5, Unpaired, 2-tailed t -test, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Expressing, Immunohistochemistry, Staining

    B1R blockade reduces reactive oxygen species (ROS) production in the kidney and HK-2 cells. (A) Representative photomicrographs showing dihydroethidium (DHE) staining in the kidney sections. (B) DHE staining quantified as relative fluorescence intensity showing increased superoxide generation in the kidneys of DOCA-salt treated hypertensive mice compared with sham treated wild-type (WT) mice. This increase in DHE staining was blunted in B1R deficient mice (B1RKO) mice with DOCA-salt treatment ( n = 6, Two-way ANOVA, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R blockade reduces reactive oxygen species (ROS) production in the kidney and HK-2 cells. (A) Representative photomicrographs showing dihydroethidium (DHE) staining in the kidney sections. (B) DHE staining quantified as relative fluorescence intensity showing increased superoxide generation in the kidneys of DOCA-salt treated hypertensive mice compared with sham treated wild-type (WT) mice. This increase in DHE staining was blunted in B1R deficient mice (B1RKO) mice with DOCA-salt treatment ( n = 6, Two-way ANOVA, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Staining, Fluorescence, Mouse Assay

    B1R gene deletion prevents gene expression of renal fibrosis markers in DOCA-salt hypertension. Gene expression measured by real time RT-PCR showing significantly increased mRNA of renal fibrosis markers in the kidney cortex of DOCA-salt treated hypertensive mice compared with sham mice. B1R knockout mice did not show this DOCA-salt-induced increase in renal fibrosis markers. Data was normalized to β-actin and presented as mean ± SEM ( n = 6, Two-way ANOVA, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R gene deletion prevents gene expression of renal fibrosis markers in DOCA-salt hypertension. Gene expression measured by real time RT-PCR showing significantly increased mRNA of renal fibrosis markers in the kidney cortex of DOCA-salt treated hypertensive mice compared with sham mice. B1R knockout mice did not show this DOCA-salt-induced increase in renal fibrosis markers. Data was normalized to β-actin and presented as mean ± SEM ( n = 6, Two-way ANOVA, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Expressing, Quantitative RT-PCR, Mouse Assay, Knock-Out

    B1R gene deletion abrogates DOCA-salt induced renal myofibroblast transition. (A) Representative immunofluorescence images showing expression of alpha-smooth muscle actin (α-SMA), fibronectin, and transforming growth factor-beta (TGF-β) in the kidney sections. Quantification data presented as mean fluorescence staining showing increased expression of α-SMA (B) , fibronectin (C) , and TGF-β (D) of DOCA-salt treated hypertensive mice compared with sham mice. These increases in fibrosis markers expression were blunted in B1R deficient mice with 3 weeks of DOCA-salt treatment ( n = 6, Two-way ANOVA, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R gene deletion abrogates DOCA-salt induced renal myofibroblast transition. (A) Representative immunofluorescence images showing expression of alpha-smooth muscle actin (α-SMA), fibronectin, and transforming growth factor-beta (TGF-β) in the kidney sections. Quantification data presented as mean fluorescence staining showing increased expression of α-SMA (B) , fibronectin (C) , and TGF-β (D) of DOCA-salt treated hypertensive mice compared with sham mice. These increases in fibrosis markers expression were blunted in B1R deficient mice with 3 weeks of DOCA-salt treatment ( n = 6, Two-way ANOVA, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Immunofluorescence, Expressing, Fluorescence, Staining, Mouse Assay

    B1R gene deletion prevents kidney injury in DOCA-salt hypertension. (A) Representative immunofluorescence images showing expression of kidney injury molecule-1 (Kim-1) in the kidney sections. (B) Quantification data presented as mean fluorescence staining showing increased expression of Kim-1 in the kidneys of DOCA-salt treated hypertensive mice compared with sham treated wild-type (WT) mice. This increase in Kim-1 expression was blunted in B1R deficient mice (B1RKO) mice with DOCA-salt treatment ( n = 5, Two-way ANOVA, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R gene deletion prevents kidney injury in DOCA-salt hypertension. (A) Representative immunofluorescence images showing expression of kidney injury molecule-1 (Kim-1) in the kidney sections. (B) Quantification data presented as mean fluorescence staining showing increased expression of Kim-1 in the kidneys of DOCA-salt treated hypertensive mice compared with sham treated wild-type (WT) mice. This increase in Kim-1 expression was blunted in B1R deficient mice (B1RKO) mice with DOCA-salt treatment ( n = 5, Two-way ANOVA, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Immunofluorescence, Expressing, Fluorescence, Staining, Mouse Assay

    B1R expression in human kidney proximal tubular epithelial (HK-2) cells. (A) Representative photomicrographs showing immunofluorescence of B1R in HK-2 cells treated vehicle or B1R specific agonist DAKD for 24 h. Control HK-2 cells without primary antibody (No 1°Ab control) incubation and with only secondary antibody incubation shows no staining. (B) The quantification of B1R immunoreactivity shows that the DAKD treatment of HK-2 cells for 24 h significantly upregulated the B1R expression ( n =7–8, Unpaired, 2-tailed t -test, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: B1R expression in human kidney proximal tubular epithelial (HK-2) cells. (A) Representative photomicrographs showing immunofluorescence of B1R in HK-2 cells treated vehicle or B1R specific agonist DAKD for 24 h. Control HK-2 cells without primary antibody (No 1°Ab control) incubation and with only secondary antibody incubation shows no staining. (B) The quantification of B1R immunoreactivity shows that the DAKD treatment of HK-2 cells for 24 h significantly upregulated the B1R expression ( n =7–8, Unpaired, 2-tailed t -test, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Expressing, Immunofluorescence, Incubation, Staining

    Elevated B1R expression in the kidneys of DOCA-salt hypertensive mice. (A) Gene expression measured by real time RT-PCR showing significantly increased mRNA in the kidneys at 7, 14, and 21 days of DOCA-salt treated hypertensive mice compared with sham mice ( n = 6, One-way ANOVA, * P

    Journal: Frontiers in Medicine

    Article Title: Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension

    doi: 10.3389/fmed.2021.780834

    Figure Lengend Snippet: Elevated B1R expression in the kidneys of DOCA-salt hypertensive mice. (A) Gene expression measured by real time RT-PCR showing significantly increased mRNA in the kidneys at 7, 14, and 21 days of DOCA-salt treated hypertensive mice compared with sham mice ( n = 6, One-way ANOVA, * P

    Article Snippet: Then sections were incubated with KIM-1 (ab47635, lot #GR3295411-1, abcam), Fibronectin (ab2413, lot #GR3274504-2, abcam), α-SMA (ab5694, lot #GR3183259-32, abcam), TGF-β (ab92468, lot #GR3203762-5, abcam), B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) antibodies at 4°C overnight.

    Techniques: Expressing, Mouse Assay, Quantitative RT-PCR