bovine pulmonary artery endothelial cells paec Search Results


c pae  (ATCC)
94
ATCC c pae
C Pae, supplied by ATCC, 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/product/bovine+pulmonary+artery+endothelial+cells+paec/CPAE/us07387779-1707-12-41
Average 94 stars, based on 1 article reviews
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primary bovine pulmonary artery endothelial cells paecs  (Cell Applications Inc)
94
Cell Applications Inc 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.
Primary Bovine Pulmonary Artery Endothelial Cells Paecs, supplied by Cell Applications Inc, 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/product/bovine+pulmonary+artery+endothelial+cells+paec/Bovine+Endothelial+Cell+Media/pmc04246092-171-0-10
Average 94 stars, based on 1 article reviews
primary bovine pulmonary artery endothelial cells paecs - by Bioz Stars, 2026-10
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pulmonary artery endothelial cell line  (ATCC)
94
ATCC pulmonary artery endothelial cell line
FIG. 1. A, expression of annexin II and p11 in cultured bovine pulmonary <t>endothelial</t> (CPAE) and Madin-Darby canine kidney (MDCK) cells. Identical amounts of total cellular protein extracted from CPAE (lanes 1 and 3) and MDCK cells (lanes 2 and 4) were separated in SDS-15% polyacrylamide gels, transferred to nitrocellulose, and analyzed by immunoblotting with monoclonal antibodies against annexin II (lanes 1 and 2) and p11 (lanes 3 and 4), respectively. The migration position of marker proteins of the molecular masses indicated (in kDa) are given on the right. B, time course of the 360-nm fluorescence intensity due to loading of a CPAE cell with 200 mM Fura-II-5 K1 salt after breaking the cell membrane. The time constant, obtained from a monoexponential fit, was 107 s.
Pulmonary Artery Endothelial Cell Line, supplied by ATCC, 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/product/bovine+pulmonary+artery+endothelial+cells+paec/CPAE%3B+Artery+Endothelium%3B+Bovine/pm08940038-28-5-11
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pulmonary artery endothelial cell line - by Bioz Stars, 2026-10
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bovine pulmonary artery endothelial cells paec  (Cell Applications Inc)
93
Cell Applications Inc bovine pulmonary artery endothelial cells paec
FIG. 1. A, expression of annexin II and p11 in cultured bovine pulmonary <t>endothelial</t> (CPAE) and Madin-Darby canine kidney (MDCK) cells. Identical amounts of total cellular protein extracted from CPAE (lanes 1 and 3) and MDCK cells (lanes 2 and 4) were separated in SDS-15% polyacrylamide gels, transferred to nitrocellulose, and analyzed by immunoblotting with monoclonal antibodies against annexin II (lanes 1 and 2) and p11 (lanes 3 and 4), respectively. The migration position of marker proteins of the molecular masses indicated (in kDa) are given on the right. B, time course of the 360-nm fluorescence intensity due to loading of a CPAE cell with 200 mM Fura-II-5 K1 salt after breaking the cell membrane. The time constant, obtained from a monoexponential fit, was 107 s.
Bovine Pulmonary Artery Endothelial Cells Paec, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/bovine+pulmonary+artery+endothelial+cells+paec/Bovine+Pulmonary+Artery+Endothelial+Cells%3A+BPAEC/pmc03006264-104-0-9
Average 93 stars, based on 1 article reviews
bovine pulmonary artery endothelial cells paec - by Bioz Stars, 2026-10
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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: 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: 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: 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: 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: Primary bovine pulmonary artery endothelial cells (PAECs) were obtained from Cell Applications (San Diego, CA).

Techniques: Control, Activity Assay, Western Blot

FIG. 1. A, expression of annexin II and p11 in cultured bovine pulmonary endothelial (CPAE) and Madin-Darby canine kidney (MDCK) cells. Identical amounts of total cellular protein extracted from CPAE (lanes 1 and 3) and MDCK cells (lanes 2 and 4) were separated in SDS-15% polyacrylamide gels, transferred to nitrocellulose, and analyzed by immunoblotting with monoclonal antibodies against annexin II (lanes 1 and 2) and p11 (lanes 3 and 4), respectively. The migration position of marker proteins of the molecular masses indicated (in kDa) are given on the right. B, time course of the 360-nm fluorescence intensity due to loading of a CPAE cell with 200 mM Fura-II-5 K1 salt after breaking the cell membrane. The time constant, obtained from a monoexponential fit, was 107 s.

Journal: The Journal of biological chemistry

Article Title: Annexin II modulates volume-activated chloride currents in vascular endothelial cells.

doi: 10.1074/jbc.271.48.30631

Figure Lengend Snippet: FIG. 1. A, expression of annexin II and p11 in cultured bovine pulmonary endothelial (CPAE) and Madin-Darby canine kidney (MDCK) cells. Identical amounts of total cellular protein extracted from CPAE (lanes 1 and 3) and MDCK cells (lanes 2 and 4) were separated in SDS-15% polyacrylamide gels, transferred to nitrocellulose, and analyzed by immunoblotting with monoclonal antibodies against annexin II (lanes 1 and 2) and p11 (lanes 3 and 4), respectively. The migration position of marker proteins of the molecular masses indicated (in kDa) are given on the right. B, time course of the 360-nm fluorescence intensity due to loading of a CPAE cell with 200 mM Fura-II-5 K1 salt after breaking the cell membrane. The time constant, obtained from a monoexponential fit, was 107 s.

Article Snippet: Cells from a cultured bovine pulmonary artery endothelial cell line (CPAE,1 ATCC CCL 209) were used.

Techniques: Expressing, Cell Culture, Western Blot, Bioprocessing, Migration, Marker, Fluorescence, Membrane