aqp4  (Alomone Labs)


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    Alomone Labs aqp4
    Hypertension induces brain Aβ deposition and glymphatic clearance impairment. (a–d) In vivo imaging of Aβ deposition in the cerebral cortex. Aβ deposition (FSB, green) was distinct along the vessels. (e) Enlarged VRS were observed. (f) 3D reconstruction of the vasculature in hypertension mice. The warping vessel is magnified on the right panel. (g-j) Ang-II evoked a significant increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) with no changes in heart rates (HR) and body weight (k-m). Glymphatic clearance impairment was evident in hypertension models. (n-o) Arterial diameters remained unchanged in hypertension models while vascular pulsatility was severely reduced (n=8-9 vessels per group) (s) . (q) Representative images of GFAP expression and <t>AQP4</t> polarization in the cortex. No distinctive changes in AQP4 polarization (t) and GFAP expression (u) were observed in the hypertension model. (p, upper panel) Representative images of smooth muscle actin (SMA) and collagen expression in the cortex. No significant changes in SMA expression (r) and greater deposition of collagen (r) in vascular walls were observed in hypertension models. (p, lower panel) Immunology of Aβ 1–40 and Aβ 1–42 in hypertension model mice. Significant deposition of Aβ 1–40, but not Aβ 1–42, in vessels was observed. (p, lower panel) Co-labeling of collagen and Aβ 1–40 in hypertension. Aβ 1–40 co-localized with collagen (n=5-6 mice per group).
    Aqp4, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aqp4/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    aqp4 - by Bioz Stars, 2022-08
    92/100 stars

    Images

    1) Product Images from "Glutamate and γ-aminobutyric acid differentially modulate glymphatic clearance of amyloid β through pulsation- and aquaporin-4 dependent mechanisms"

    Article Title: Glutamate and γ-aminobutyric acid differentially modulate glymphatic clearance of amyloid β through pulsation- and aquaporin-4 dependent mechanisms

    Journal: bioRxiv

    doi: 10.1101/2020.01.31.928481

    Hypertension induces brain Aβ deposition and glymphatic clearance impairment. (a–d) In vivo imaging of Aβ deposition in the cerebral cortex. Aβ deposition (FSB, green) was distinct along the vessels. (e) Enlarged VRS were observed. (f) 3D reconstruction of the vasculature in hypertension mice. The warping vessel is magnified on the right panel. (g-j) Ang-II evoked a significant increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) with no changes in heart rates (HR) and body weight (k-m). Glymphatic clearance impairment was evident in hypertension models. (n-o) Arterial diameters remained unchanged in hypertension models while vascular pulsatility was severely reduced (n=8-9 vessels per group) (s) . (q) Representative images of GFAP expression and AQP4 polarization in the cortex. No distinctive changes in AQP4 polarization (t) and GFAP expression (u) were observed in the hypertension model. (p, upper panel) Representative images of smooth muscle actin (SMA) and collagen expression in the cortex. No significant changes in SMA expression (r) and greater deposition of collagen (r) in vascular walls were observed in hypertension models. (p, lower panel) Immunology of Aβ 1–40 and Aβ 1–42 in hypertension model mice. Significant deposition of Aβ 1–40, but not Aβ 1–42, in vessels was observed. (p, lower panel) Co-labeling of collagen and Aβ 1–40 in hypertension. Aβ 1–40 co-localized with collagen (n=5-6 mice per group).
    Figure Legend Snippet: Hypertension induces brain Aβ deposition and glymphatic clearance impairment. (a–d) In vivo imaging of Aβ deposition in the cerebral cortex. Aβ deposition (FSB, green) was distinct along the vessels. (e) Enlarged VRS were observed. (f) 3D reconstruction of the vasculature in hypertension mice. The warping vessel is magnified on the right panel. (g-j) Ang-II evoked a significant increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) with no changes in heart rates (HR) and body weight (k-m). Glymphatic clearance impairment was evident in hypertension models. (n-o) Arterial diameters remained unchanged in hypertension models while vascular pulsatility was severely reduced (n=8-9 vessels per group) (s) . (q) Representative images of GFAP expression and AQP4 polarization in the cortex. No distinctive changes in AQP4 polarization (t) and GFAP expression (u) were observed in the hypertension model. (p, upper panel) Representative images of smooth muscle actin (SMA) and collagen expression in the cortex. No significant changes in SMA expression (r) and greater deposition of collagen (r) in vascular walls were observed in hypertension models. (p, lower panel) Immunology of Aβ 1–40 and Aβ 1–42 in hypertension model mice. Significant deposition of Aβ 1–40, but not Aβ 1–42, in vessels was observed. (p, lower panel) Co-labeling of collagen and Aβ 1–40 in hypertension. Aβ 1–40 co-localized with collagen (n=5-6 mice per group).

    Techniques Used: In Vivo Imaging, Mouse Assay, Expressing, Labeling

    Impairment of glymphatic clearance and deposition of Aβ plaques in APP-PS1 mice. (a) In vivo imaging of Aβ deposition in the cerebral cortex (FSB: green). Aβ deposition was evident in the parenchyma with no distinct CAA. (b) Immunology of Aβ 1–40 and Aβ 1–42 in APP-PS1. Significant numbers of Aβ 1–42-labeled amyloid plaques were observed in the parenchyma, but no marked deposition of Aβ 1–40. (c) Representative images of paravascular CSF tracer clearance at 100 μm below the cortical surface in APP-PS1 indicating severe impairment in penetration of fluorescence tracer (e) while no changes in paravascular movement was observed (d). (h-i) Expression of AQP4 and GFAP in cortex and hippocampus. Compared with WT control mice, APP-PS1 mice displayed significant decrease in AQP4 polarization and exhibited a marked increase in GFAP expression in the cortex (n=6 mice per group). No significant pulsatility changes were observed between APP-PS1 and WT control mice (f) (n=7-8 vessels per group).
    Figure Legend Snippet: Impairment of glymphatic clearance and deposition of Aβ plaques in APP-PS1 mice. (a) In vivo imaging of Aβ deposition in the cerebral cortex (FSB: green). Aβ deposition was evident in the parenchyma with no distinct CAA. (b) Immunology of Aβ 1–40 and Aβ 1–42 in APP-PS1. Significant numbers of Aβ 1–42-labeled amyloid plaques were observed in the parenchyma, but no marked deposition of Aβ 1–40. (c) Representative images of paravascular CSF tracer clearance at 100 μm below the cortical surface in APP-PS1 indicating severe impairment in penetration of fluorescence tracer (e) while no changes in paravascular movement was observed (d). (h-i) Expression of AQP4 and GFAP in cortex and hippocampus. Compared with WT control mice, APP-PS1 mice displayed significant decrease in AQP4 polarization and exhibited a marked increase in GFAP expression in the cortex (n=6 mice per group). No significant pulsatility changes were observed between APP-PS1 and WT control mice (f) (n=7-8 vessels per group).

    Techniques Used: Mouse Assay, In Vivo Imaging, Labeling, Fluorescence, Expressing

    Effects of Glutamate and GABA on tracer penetration into parenchyma are AQP4-dependent. (a) In vivo two-photon imaging of tracer clearance through the glymphatic pathway after intracisternal injection of GABA/glutamate and the respective antagonists in AQP4 -/- mice. (b, c) Quantification of CSF tracer influx into the surrounding parenchyma via 3D reconstruction and paravascular CSF tracer clearance at 100 μm below the cortical surface (d, e) . APV strongly accelerated paravasular movement while no significant changes were observed in mice receiving glutamate and CNQX. GABA and bicuculline did not affect paravascular movement. No significant changes in tracer penetration into the interstitium were observed among the experimental groups, compared with the vehicle group (n=6 mice per group).
    Figure Legend Snippet: Effects of Glutamate and GABA on tracer penetration into parenchyma are AQP4-dependent. (a) In vivo two-photon imaging of tracer clearance through the glymphatic pathway after intracisternal injection of GABA/glutamate and the respective antagonists in AQP4 -/- mice. (b, c) Quantification of CSF tracer influx into the surrounding parenchyma via 3D reconstruction and paravascular CSF tracer clearance at 100 μm below the cortical surface (d, e) . APV strongly accelerated paravasular movement while no significant changes were observed in mice receiving glutamate and CNQX. GABA and bicuculline did not affect paravascular movement. No significant changes in tracer penetration into the interstitium were observed among the experimental groups, compared with the vehicle group (n=6 mice per group).

    Techniques Used: In Vivo, Imaging, Injection, Mouse Assay

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    Alomone Labs anti aqp4
    The synthesized GILZ-p inhibited LPS induced Müller cell gliosis. Western blot analysis was performed to determine the protein expression levels of glial fibrillary acidic protein (GFAP) (A,B) , and <t>AQP4</t> (C,D) in Müller cells treated with 1000 ng/ml LPS in combination with different concentrations of GILZ-p (0.01, 0.1, 1, and 10 μM) for 24 h. β-actin was used as the loading control. The results of quantitative analysis, as determined by densitometric analysis, were expressed as relative to β-actin. Data represent the mean ± SE; the Mann–Whitney U -test was used for comparisons between two groups. n = 3 for each group. ∗ P
    Anti Aqp4, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti aqp4/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti aqp4 - by Bioz Stars, 2022-08
    92/100 stars
      Buy from Supplier

    95
    Alomone Labs aqp4 antibodies
    The synthesized GILZ-p inhibited LPS induced Müller cell gliosis. Western blot analysis was performed to determine the protein expression levels of glial fibrillary acidic protein (GFAP) (A,B) , and <t>AQP4</t> (C,D) in Müller cells treated with 1000 ng/ml LPS in combination with different concentrations of GILZ-p (0.01, 0.1, 1, and 10 μM) for 24 h. β-actin was used as the loading control. The results of quantitative analysis, as determined by densitometric analysis, were expressed as relative to β-actin. Data represent the mean ± SE; the Mann–Whitney U -test was used for comparisons between two groups. n = 3 for each group. ∗ P
    Aqp4 Antibodies, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aqp4 antibodies/product/Alomone Labs
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    aqp4 antibodies - by Bioz Stars, 2022-08
    95/100 stars
      Buy from Supplier

    Image Search Results


    The synthesized GILZ-p inhibited LPS induced Müller cell gliosis. Western blot analysis was performed to determine the protein expression levels of glial fibrillary acidic protein (GFAP) (A,B) , and AQP4 (C,D) in Müller cells treated with 1000 ng/ml LPS in combination with different concentrations of GILZ-p (0.01, 0.1, 1, and 10 μM) for 24 h. β-actin was used as the loading control. The results of quantitative analysis, as determined by densitometric analysis, were expressed as relative to β-actin. Data represent the mean ± SE; the Mann–Whitney U -test was used for comparisons between two groups. n = 3 for each group. ∗ P

    Journal: Frontiers in Pharmacology

    Article Title: A Synthesized Glucocorticoid- Induced Leucine Zipper Peptide Inhibits Retinal Müller Cell Gliosis

    doi: 10.3389/fphar.2018.00331

    Figure Lengend Snippet: The synthesized GILZ-p inhibited LPS induced Müller cell gliosis. Western blot analysis was performed to determine the protein expression levels of glial fibrillary acidic protein (GFAP) (A,B) , and AQP4 (C,D) in Müller cells treated with 1000 ng/ml LPS in combination with different concentrations of GILZ-p (0.01, 0.1, 1, and 10 μM) for 24 h. β-actin was used as the loading control. The results of quantitative analysis, as determined by densitometric analysis, were expressed as relative to β-actin. Data represent the mean ± SE; the Mann–Whitney U -test was used for comparisons between two groups. n = 3 for each group. ∗ P

    Article Snippet: The membranes were blocked in 5% non-fat milk at room temperature for 1 h and incubated with the following antibodies: anti-monocyte chemoattractant protein (MCP)-1 (ab25124; Abcam, Cambridge, United Kingdom), anti-intercellular adhesion molecule (ICAM)-1 (ab171123; Proteintech, Chicago, IL, United States), anti-IL1β (ab9787; Abcam), Anti-tumor necrosis factor (TNF)α (PB0270, Boster Biological Technology, Wuhan, China), rabbit anti-p65 polyclonal antibody (ab16502; Abcam), anti-phospho-NF-κB p65 (Ser536) rabbit monoclonal antibody (3033P; Cell Signaling Technology, Beverly, MA, United States), anti-AQP4 (300-314, Alomone Labs, Jerusalem, Israel), anti-glial fibrillary acidic protein (GFAP) (ab10062, Abcam), or rabbit anti β-actin antibody (ab69512; Abcam) overnight.

    Techniques: Synthesized, Western Blot, Expressing, MANN-WHITNEY

    Hypertension induces brain Aβ deposition and glymphatic clearance impairment. (a–d) In vivo imaging of Aβ deposition in the cerebral cortex. Aβ deposition (FSB, green) was distinct along the vessels. (e) Enlarged VRS were observed. (f) 3D reconstruction of the vasculature in hypertension mice. The warping vessel is magnified on the right panel. (g-j) Ang-II evoked a significant increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) with no changes in heart rates (HR) and body weight (k-m). Glymphatic clearance impairment was evident in hypertension models. (n-o) Arterial diameters remained unchanged in hypertension models while vascular pulsatility was severely reduced (n=8-9 vessels per group) (s) . (q) Representative images of GFAP expression and AQP4 polarization in the cortex. No distinctive changes in AQP4 polarization (t) and GFAP expression (u) were observed in the hypertension model. (p, upper panel) Representative images of smooth muscle actin (SMA) and collagen expression in the cortex. No significant changes in SMA expression (r) and greater deposition of collagen (r) in vascular walls were observed in hypertension models. (p, lower panel) Immunology of Aβ 1–40 and Aβ 1–42 in hypertension model mice. Significant deposition of Aβ 1–40, but not Aβ 1–42, in vessels was observed. (p, lower panel) Co-labeling of collagen and Aβ 1–40 in hypertension. Aβ 1–40 co-localized with collagen (n=5-6 mice per group).

    Journal: bioRxiv

    Article Title: Glutamate and γ-aminobutyric acid differentially modulate glymphatic clearance of amyloid β through pulsation- and aquaporin-4 dependent mechanisms

    doi: 10.1101/2020.01.31.928481

    Figure Lengend Snippet: Hypertension induces brain Aβ deposition and glymphatic clearance impairment. (a–d) In vivo imaging of Aβ deposition in the cerebral cortex. Aβ deposition (FSB, green) was distinct along the vessels. (e) Enlarged VRS were observed. (f) 3D reconstruction of the vasculature in hypertension mice. The warping vessel is magnified on the right panel. (g-j) Ang-II evoked a significant increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) with no changes in heart rates (HR) and body weight (k-m). Glymphatic clearance impairment was evident in hypertension models. (n-o) Arterial diameters remained unchanged in hypertension models while vascular pulsatility was severely reduced (n=8-9 vessels per group) (s) . (q) Representative images of GFAP expression and AQP4 polarization in the cortex. No distinctive changes in AQP4 polarization (t) and GFAP expression (u) were observed in the hypertension model. (p, upper panel) Representative images of smooth muscle actin (SMA) and collagen expression in the cortex. No significant changes in SMA expression (r) and greater deposition of collagen (r) in vascular walls were observed in hypertension models. (p, lower panel) Immunology of Aβ 1–40 and Aβ 1–42 in hypertension model mice. Significant deposition of Aβ 1–40, but not Aβ 1–42, in vessels was observed. (p, lower panel) Co-labeling of collagen and Aβ 1–40 in hypertension. Aβ 1–40 co-localized with collagen (n=5-6 mice per group).

    Article Snippet: Antibodies for Collagen-I (Co-I) (Abcam, ab34710, Hong Kong, UK) and α-smooth muscle actin (SMA) (Boster, BM0002, Wuhan, China) were used to test vascular structure changes and those for AQP4 (Alomone Labs, 300-314, Jerusalem, Israel) and GFAP (Millipore, 2642205, USA) to detect aquaporin and astrocytes, respectively.

    Techniques: In Vivo Imaging, Mouse Assay, Expressing, Labeling

    Impairment of glymphatic clearance and deposition of Aβ plaques in APP-PS1 mice. (a) In vivo imaging of Aβ deposition in the cerebral cortex (FSB: green). Aβ deposition was evident in the parenchyma with no distinct CAA. (b) Immunology of Aβ 1–40 and Aβ 1–42 in APP-PS1. Significant numbers of Aβ 1–42-labeled amyloid plaques were observed in the parenchyma, but no marked deposition of Aβ 1–40. (c) Representative images of paravascular CSF tracer clearance at 100 μm below the cortical surface in APP-PS1 indicating severe impairment in penetration of fluorescence tracer (e) while no changes in paravascular movement was observed (d). (h-i) Expression of AQP4 and GFAP in cortex and hippocampus. Compared with WT control mice, APP-PS1 mice displayed significant decrease in AQP4 polarization and exhibited a marked increase in GFAP expression in the cortex (n=6 mice per group). No significant pulsatility changes were observed between APP-PS1 and WT control mice (f) (n=7-8 vessels per group).

    Journal: bioRxiv

    Article Title: Glutamate and γ-aminobutyric acid differentially modulate glymphatic clearance of amyloid β through pulsation- and aquaporin-4 dependent mechanisms

    doi: 10.1101/2020.01.31.928481

    Figure Lengend Snippet: Impairment of glymphatic clearance and deposition of Aβ plaques in APP-PS1 mice. (a) In vivo imaging of Aβ deposition in the cerebral cortex (FSB: green). Aβ deposition was evident in the parenchyma with no distinct CAA. (b) Immunology of Aβ 1–40 and Aβ 1–42 in APP-PS1. Significant numbers of Aβ 1–42-labeled amyloid plaques were observed in the parenchyma, but no marked deposition of Aβ 1–40. (c) Representative images of paravascular CSF tracer clearance at 100 μm below the cortical surface in APP-PS1 indicating severe impairment in penetration of fluorescence tracer (e) while no changes in paravascular movement was observed (d). (h-i) Expression of AQP4 and GFAP in cortex and hippocampus. Compared with WT control mice, APP-PS1 mice displayed significant decrease in AQP4 polarization and exhibited a marked increase in GFAP expression in the cortex (n=6 mice per group). No significant pulsatility changes were observed between APP-PS1 and WT control mice (f) (n=7-8 vessels per group).

    Article Snippet: Antibodies for Collagen-I (Co-I) (Abcam, ab34710, Hong Kong, UK) and α-smooth muscle actin (SMA) (Boster, BM0002, Wuhan, China) were used to test vascular structure changes and those for AQP4 (Alomone Labs, 300-314, Jerusalem, Israel) and GFAP (Millipore, 2642205, USA) to detect aquaporin and astrocytes, respectively.

    Techniques: Mouse Assay, In Vivo Imaging, Labeling, Fluorescence, Expressing

    Effects of Glutamate and GABA on tracer penetration into parenchyma are AQP4-dependent. (a) In vivo two-photon imaging of tracer clearance through the glymphatic pathway after intracisternal injection of GABA/glutamate and the respective antagonists in AQP4 -/- mice. (b, c) Quantification of CSF tracer influx into the surrounding parenchyma via 3D reconstruction and paravascular CSF tracer clearance at 100 μm below the cortical surface (d, e) . APV strongly accelerated paravasular movement while no significant changes were observed in mice receiving glutamate and CNQX. GABA and bicuculline did not affect paravascular movement. No significant changes in tracer penetration into the interstitium were observed among the experimental groups, compared with the vehicle group (n=6 mice per group).

    Journal: bioRxiv

    Article Title: Glutamate and γ-aminobutyric acid differentially modulate glymphatic clearance of amyloid β through pulsation- and aquaporin-4 dependent mechanisms

    doi: 10.1101/2020.01.31.928481

    Figure Lengend Snippet: Effects of Glutamate and GABA on tracer penetration into parenchyma are AQP4-dependent. (a) In vivo two-photon imaging of tracer clearance through the glymphatic pathway after intracisternal injection of GABA/glutamate and the respective antagonists in AQP4 -/- mice. (b, c) Quantification of CSF tracer influx into the surrounding parenchyma via 3D reconstruction and paravascular CSF tracer clearance at 100 μm below the cortical surface (d, e) . APV strongly accelerated paravasular movement while no significant changes were observed in mice receiving glutamate and CNQX. GABA and bicuculline did not affect paravascular movement. No significant changes in tracer penetration into the interstitium were observed among the experimental groups, compared with the vehicle group (n=6 mice per group).

    Article Snippet: Antibodies for Collagen-I (Co-I) (Abcam, ab34710, Hong Kong, UK) and α-smooth muscle actin (SMA) (Boster, BM0002, Wuhan, China) were used to test vascular structure changes and those for AQP4 (Alomone Labs, 300-314, Jerusalem, Israel) and GFAP (Millipore, 2642205, USA) to detect aquaporin and astrocytes, respectively.

    Techniques: In Vivo, Imaging, Injection, Mouse Assay

    The synthesized GILZ-p inhibited LPS induced Müller cell gliosis. Western blot analysis was performed to determine the protein expression levels of glial fibrillary acidic protein (GFAP) (A,B) , and AQP4 (C,D) in Müller cells treated with 1000 ng/ml LPS in combination with different concentrations of GILZ-p (0.01, 0.1, 1, and 10 μM) for 24 h. β-actin was used as the loading control. The results of quantitative analysis, as determined by densitometric analysis, were expressed as relative to β-actin. Data represent the mean ± SE; the Mann–Whitney U -test was used for comparisons between two groups. n = 3 for each group. ∗ P

    Journal: Frontiers in Pharmacology

    Article Title: A Synthesized Glucocorticoid- Induced Leucine Zipper Peptide Inhibits Retinal Müller Cell Gliosis

    doi: 10.3389/fphar.2018.00331

    Figure Lengend Snippet: The synthesized GILZ-p inhibited LPS induced Müller cell gliosis. Western blot analysis was performed to determine the protein expression levels of glial fibrillary acidic protein (GFAP) (A,B) , and AQP4 (C,D) in Müller cells treated with 1000 ng/ml LPS in combination with different concentrations of GILZ-p (0.01, 0.1, 1, and 10 μM) for 24 h. β-actin was used as the loading control. The results of quantitative analysis, as determined by densitometric analysis, were expressed as relative to β-actin. Data represent the mean ± SE; the Mann–Whitney U -test was used for comparisons between two groups. n = 3 for each group. ∗ P

    Article Snippet: The membranes were blocked in 5% non-fat milk at room temperature for 1 h and incubated with the following antibodies: anti-monocyte chemoattractant protein (MCP)-1 (ab25124; Abcam, Cambridge, United Kingdom), anti-intercellular adhesion molecule (ICAM)-1 (ab171123; Proteintech, Chicago, IL, United States), anti-IL1β (ab9787; Abcam), Anti-tumor necrosis factor (TNF)α (PB0270, Boster Biological Technology, Wuhan, China), rabbit anti-p65 polyclonal antibody (ab16502; Abcam), anti-phospho-NF-κB p65 (Ser536) rabbit monoclonal antibody (3033P; Cell Signaling Technology, Beverly, MA, United States), anti-AQP4 (300-314, Alomone Labs, Jerusalem, Israel), anti-glial fibrillary acidic protein (GFAP) (ab10062, Abcam), or rabbit anti β-actin antibody (ab69512; Abcam) overnight.

    Techniques: Synthesized, Western Blot, Expressing, MANN-WHITNEY