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cell culture primary bovine pulmonary artery endothelial cells paecs  (Cell Applications Inc)


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    Cell Applications Inc cell culture primary bovine pulmonary artery endothelial cells paecs
    l-NAME attenuates hyperoxia-induced disruption of <t>endothelial</t> monolayer barrier integrity. <t>PAECs</t> were treated with and without l-NAME (3 mm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under normoxia and hyperoxia. B, changes in TEER of endothelial monolayer under hyperoxia with and without l-NAME. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus l-NAME+normoxia; **, p < 0.05 versus control hyperoxia.
    Cell Culture Primary Bovine Pulmonary Artery Endothelial Cells Paecs, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 95/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cell culture primary bovine pulmonary artery endothelial cells paecs/product/Cell Applications Inc
    Average 95 stars, based on 13 article reviews
    cell culture primary bovine pulmonary artery endothelial cells paecs - by Bioz Stars, 2026-02
    95/100 stars

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    1) Product Images from "Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation * "

    Article Title: Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M114.585356

    l-NAME attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with and without l-NAME (3 mm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under normoxia and hyperoxia. B, changes in TEER of endothelial monolayer under hyperoxia with and without l-NAME. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus l-NAME+normoxia; **, p < 0.05 versus control hyperoxia.
    Figure Legend Snippet: l-NAME attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with and without l-NAME (3 mm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under normoxia and hyperoxia. B, changes in TEER of endothelial monolayer under hyperoxia with and without l-NAME. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus l-NAME+normoxia; **, p < 0.05 versus control hyperoxia.

    Techniques Used: Disruption, Control

    Uric acid prevents hyperoxia-induced disruption of lung endothelial barrier in the second phase and apoptosis. PAECs were treated with and without uric acid (3 mm) and exposed to hyperoxia for 48 h, during which TEER was continuously monitored. After exposure, apoptotic cells were detected using TUNEL assay as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer. B, alterations in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus UA+normoxia; **, p < 0.05 versus hyperoxia. UA = uric acid.
    Figure Legend Snippet: Uric acid prevents hyperoxia-induced disruption of lung endothelial barrier in the second phase and apoptosis. PAECs were treated with and without uric acid (3 mm) and exposed to hyperoxia for 48 h, during which TEER was continuously monitored. After exposure, apoptotic cells were detected using TUNEL assay as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer. B, alterations in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus UA+normoxia; **, p < 0.05 versus hyperoxia. UA = uric acid.

    Techniques Used: Disruption, TUNEL Assay

    Peptide P326TAT attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under hyperoxia with control peptide PlwTAT. B, changes in TEER of endothelial monolayer under hyperoxia with P326TAT. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus P326TAT+normoxia or PlwTAT+normoxia; **, p < 0.05 versus hyperoxia.
    Figure Legend Snippet: Peptide P326TAT attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under hyperoxia with control peptide PlwTAT. B, changes in TEER of endothelial monolayer under hyperoxia with P326TAT. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus P326TAT+normoxia or PlwTAT+normoxia; **, p < 0.05 versus hyperoxia.

    Techniques Used: Disruption, Control

    Peptide P326TAT attenuates hyperoxia-induced apoptosis of lung endothelial cells. PAECs were exposed to hyperoxia or normoxia in the presence of P326TAT (20 μm) or control peptide PlwTAT (20 μm) for 48 h, and then apoptosis was evaluated using TUNEL assay. A, representative images of TUNEL staining. WO peptide, without peptide. B, bar graph depicting the changes in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus PlwTAT+hyperoxia or hyperoxia only.
    Figure Legend Snippet: Peptide P326TAT attenuates hyperoxia-induced apoptosis of lung endothelial cells. PAECs were exposed to hyperoxia or normoxia in the presence of P326TAT (20 μm) or control peptide PlwTAT (20 μm) for 48 h, and then apoptosis was evaluated using TUNEL assay. A, representative images of TUNEL staining. WO peptide, without peptide. B, bar graph depicting the changes in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus PlwTAT+hyperoxia or hyperoxia only.

    Techniques Used: Control, TUNEL Assay, Staining

    Peptide P326TAT prevents both caspase-dependent and caspase-independent apoptosis of lung endothelial cells. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h, after which caspase-3 activity and AIF protein level in the nuclear fraction were measured as described under “Experimental Procedures.” A, changes in caspase-3 activity. B, representative image of Western blot of AIF. WO peptide, without peptide. C, bar graph depicting changes in nuclear AIF levels of PAECs. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia.
    Figure Legend Snippet: Peptide P326TAT prevents both caspase-dependent and caspase-independent apoptosis of lung endothelial cells. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h, after which caspase-3 activity and AIF protein level in the nuclear fraction were measured as described under “Experimental Procedures.” A, changes in caspase-3 activity. B, representative image of Western blot of AIF. WO peptide, without peptide. C, bar graph depicting changes in nuclear AIF levels of PAECs. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia.

    Techniques Used: Control, Activity Assay, Western Blot



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    cell culture primary bovine pulmonary artery endothelial cells paecs  (Cell Applications Inc)
    95
    Cell Applications Inc cell culture primary bovine pulmonary artery endothelial cells paecs
    l-NAME attenuates hyperoxia-induced disruption of <t>endothelial</t> monolayer barrier integrity. <t>PAECs</t> were treated with and without l-NAME (3 mm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under normoxia and hyperoxia. B, changes in TEER of endothelial monolayer under hyperoxia with and without l-NAME. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus l-NAME+normoxia; **, p < 0.05 versus control hyperoxia.
    Cell Culture Primary Bovine Pulmonary Artery Endothelial Cells Paecs, supplied by Cell Applications Inc, 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/cell culture primary bovine pulmonary artery endothelial cells paecs/product/Cell Applications Inc
    Average 95 stars, based on 1 article reviews
    cell culture primary bovine pulmonary artery endothelial cells paecs - by Bioz Stars, 2026-02
    95/100 stars
    		  Buy from Supplier

    Image Search Results


    l-NAME attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with and without l-NAME (3 mm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under normoxia and hyperoxia. B, changes in TEER of endothelial monolayer under hyperoxia with and without l-NAME. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus l-NAME+normoxia; **, p < 0.05 versus control hyperoxia.

    Journal: The Journal of Biological Chemistry

    Article Title: Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation *

    doi: 10.1074/jbc.M114.585356

    Figure Lengend Snippet: l-NAME attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with and without l-NAME (3 mm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under normoxia and hyperoxia. B, changes in TEER of endothelial monolayer under hyperoxia with and without l-NAME. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus l-NAME+normoxia; **, p < 0.05 versus control hyperoxia.

    Article Snippet: Cell Culture Primary bovine pulmonary artery endothelial cells (PAECs) were obtained from Cell Applications (San Diego, CA).

    Techniques: Disruption, Control

    Uric acid prevents hyperoxia-induced disruption of lung endothelial barrier in the second phase and apoptosis. PAECs were treated with and without uric acid (3 mm) and exposed to hyperoxia for 48 h, during which TEER was continuously monitored. After exposure, apoptotic cells were detected using TUNEL assay as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer. B, alterations in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus UA+normoxia; **, p < 0.05 versus hyperoxia. UA = uric acid.

    Journal: The Journal of Biological Chemistry

    Article Title: Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation *

    doi: 10.1074/jbc.M114.585356

    Figure Lengend Snippet: Uric acid prevents hyperoxia-induced disruption of lung endothelial barrier in the second phase and apoptosis. PAECs were treated with and without uric acid (3 mm) and exposed to hyperoxia for 48 h, during which TEER was continuously monitored. After exposure, apoptotic cells were detected using TUNEL assay as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer. B, alterations in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus UA+normoxia; **, p < 0.05 versus hyperoxia. UA = uric acid.

    Article Snippet: Cell Culture Primary bovine pulmonary artery endothelial cells (PAECs) were obtained from Cell Applications (San Diego, CA).

    Techniques: Disruption, TUNEL Assay

    Peptide P326TAT attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under hyperoxia with control peptide PlwTAT. B, changes in TEER of endothelial monolayer under hyperoxia with P326TAT. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus P326TAT+normoxia or PlwTAT+normoxia; **, p < 0.05 versus hyperoxia.

    Journal: The Journal of Biological Chemistry

    Article Title: Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation *

    doi: 10.1074/jbc.M114.585356

    Figure Lengend Snippet: Peptide P326TAT attenuates hyperoxia-induced disruption of endothelial monolayer barrier integrity. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h. TEER was continuously monitored as described under “Experimental Procedures.” A, changes in TEER of endothelial monolayer under hyperoxia with control peptide PlwTAT. B, changes in TEER of endothelial monolayer under hyperoxia with P326TAT. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus P326TAT+normoxia or PlwTAT+normoxia; **, p < 0.05 versus hyperoxia.

    Article Snippet: Cell Culture Primary bovine pulmonary artery endothelial cells (PAECs) were obtained from Cell Applications (San Diego, CA).

    Techniques: Disruption, Control

    Peptide P326TAT attenuates hyperoxia-induced apoptosis of lung endothelial cells. PAECs were exposed to hyperoxia or normoxia in the presence of P326TAT (20 μm) or control peptide PlwTAT (20 μm) for 48 h, and then apoptosis was evaluated using TUNEL assay. A, representative images of TUNEL staining. WO peptide, without peptide. B, bar graph depicting the changes in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus PlwTAT+hyperoxia or hyperoxia only.

    Journal: The Journal of Biological Chemistry

    Article Title: Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation *

    doi: 10.1074/jbc.M114.585356

    Figure Lengend Snippet: Peptide P326TAT attenuates hyperoxia-induced apoptosis of lung endothelial cells. PAECs were exposed to hyperoxia or normoxia in the presence of P326TAT (20 μm) or control peptide PlwTAT (20 μm) for 48 h, and then apoptosis was evaluated using TUNEL assay. A, representative images of TUNEL staining. WO peptide, without peptide. B, bar graph depicting the changes in the numbers of TUNEL-positive cells. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia; #, p < 0.05 versus PlwTAT+hyperoxia or hyperoxia only.

    Article Snippet: Cell Culture Primary bovine pulmonary artery endothelial cells (PAECs) were obtained from Cell Applications (San Diego, CA).

    Techniques: Control, TUNEL Assay, Staining

    Peptide P326TAT prevents both caspase-dependent and caspase-independent apoptosis of lung endothelial cells. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h, after which caspase-3 activity and AIF protein level in the nuclear fraction were measured as described under “Experimental Procedures.” A, changes in caspase-3 activity. B, representative image of Western blot of AIF. WO peptide, without peptide. C, bar graph depicting changes in nuclear AIF levels of PAECs. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia.

    Journal: The Journal of Biological Chemistry

    Article Title: Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation *

    doi: 10.1074/jbc.M114.585356

    Figure Lengend Snippet: Peptide P326TAT prevents both caspase-dependent and caspase-independent apoptosis of lung endothelial cells. PAECs were treated with peptide P326TAT (20 μm) or control peptide PlwTAT (20 μm) and exposed to hyperoxia for 48 h, after which caspase-3 activity and AIF protein level in the nuclear fraction were measured as described under “Experimental Procedures.” A, changes in caspase-3 activity. B, representative image of Western blot of AIF. WO peptide, without peptide. C, bar graph depicting changes in nuclear AIF levels of PAECs. Results are expressed as means ± S.E.; n = 4. *, p < 0.05 versus normoxia.

    Article Snippet: Cell Culture Primary bovine pulmonary artery endothelial cells (PAECs) were obtained from Cell Applications (San Diego, CA).

    Techniques: Control, Activity Assay, Western Blot