CD39 Modulates Endothelial Cell Activation and Apoptosis

Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored...
Ausführliche Beschreibung

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Autor*in:	Goepfert, Christian [verfasserIn] Imai, Masato Brouard, Sophie Csizmadia, Eva Kaczmarek, Elzbieta Robson, Simon C.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2000

Schlagwörter:	Human Umbilical Vein Endothelial Cells (HUVEC) NTPDase Activity Noninfected Cells HUVEC Cultures Infected HUVEC

Anmerkung:	© Picower Institute Press 2000

Übergeordnetes Werk:	Enthalten in: Molecular medicine - [London] : BioMed Central, 1994, 6(2000), 7 vom: 01. Juli, Seite 591-603
Übergeordnetes Werk:	volume:6 ; year:2000 ; number:7 ; day:01 ; month:07 ; pages:591-603

Links:	Volltext

DOI / URN:	10.1007/BF03401797

Katalog-ID:	SPR008057656

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520			\|a Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications.
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700	1		\|a Imai, Masato \|4 aut
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700	1		\|a Kaczmarek, Elzbieta \|4 aut
700	1		\|a Robson, Simon C. \|4 aut
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allfields	10.1007/BF03401797 doi (DE-627)SPR008057656 (SPR)BF03401797-e DE-627 ger DE-627 rakwb eng Goepfert, Christian verfasserin aut CD39 Modulates Endothelial Cell Activation and Apoptosis 2000 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Picower Institute Press 2000 Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. Human Umbilical Vein Endothelial Cells (HUVEC) (dpeaa)DE-He213 NTPDase Activity (dpeaa)DE-He213 Noninfected Cells (dpeaa)DE-He213 HUVEC Cultures (dpeaa)DE-He213 Infected HUVEC (dpeaa)DE-He213 Imai, Masato aut Brouard, Sophie aut Csizmadia, Eva aut Kaczmarek, Elzbieta aut Robson, Simon C. aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 6(2000), 7 vom: 01. Juli, Seite 591-603 (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:6 year:2000 number:7 day:01 month:07 pages:591-603 https://dx.doi.org/10.1007/BF03401797 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2875 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2000 7 01 07 591-603
spelling	10.1007/BF03401797 doi (DE-627)SPR008057656 (SPR)BF03401797-e DE-627 ger DE-627 rakwb eng Goepfert, Christian verfasserin aut CD39 Modulates Endothelial Cell Activation and Apoptosis 2000 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Picower Institute Press 2000 Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. Human Umbilical Vein Endothelial Cells (HUVEC) (dpeaa)DE-He213 NTPDase Activity (dpeaa)DE-He213 Noninfected Cells (dpeaa)DE-He213 HUVEC Cultures (dpeaa)DE-He213 Infected HUVEC (dpeaa)DE-He213 Imai, Masato aut Brouard, Sophie aut Csizmadia, Eva aut Kaczmarek, Elzbieta aut Robson, Simon C. aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 6(2000), 7 vom: 01. Juli, Seite 591-603 (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:6 year:2000 number:7 day:01 month:07 pages:591-603 https://dx.doi.org/10.1007/BF03401797 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2875 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2000 7 01 07 591-603
allfields_unstemmed	10.1007/BF03401797 doi (DE-627)SPR008057656 (SPR)BF03401797-e DE-627 ger DE-627 rakwb eng Goepfert, Christian verfasserin aut CD39 Modulates Endothelial Cell Activation and Apoptosis 2000 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Picower Institute Press 2000 Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. Human Umbilical Vein Endothelial Cells (HUVEC) (dpeaa)DE-He213 NTPDase Activity (dpeaa)DE-He213 Noninfected Cells (dpeaa)DE-He213 HUVEC Cultures (dpeaa)DE-He213 Infected HUVEC (dpeaa)DE-He213 Imai, Masato aut Brouard, Sophie aut Csizmadia, Eva aut Kaczmarek, Elzbieta aut Robson, Simon C. aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 6(2000), 7 vom: 01. Juli, Seite 591-603 (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:6 year:2000 number:7 day:01 month:07 pages:591-603 https://dx.doi.org/10.1007/BF03401797 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2875 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2000 7 01 07 591-603
allfieldsGer	10.1007/BF03401797 doi (DE-627)SPR008057656 (SPR)BF03401797-e DE-627 ger DE-627 rakwb eng Goepfert, Christian verfasserin aut CD39 Modulates Endothelial Cell Activation and Apoptosis 2000 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Picower Institute Press 2000 Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. Human Umbilical Vein Endothelial Cells (HUVEC) (dpeaa)DE-He213 NTPDase Activity (dpeaa)DE-He213 Noninfected Cells (dpeaa)DE-He213 HUVEC Cultures (dpeaa)DE-He213 Infected HUVEC (dpeaa)DE-He213 Imai, Masato aut Brouard, Sophie aut Csizmadia, Eva aut Kaczmarek, Elzbieta aut Robson, Simon C. aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 6(2000), 7 vom: 01. Juli, Seite 591-603 (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:6 year:2000 number:7 day:01 month:07 pages:591-603 https://dx.doi.org/10.1007/BF03401797 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2875 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2000 7 01 07 591-603
allfieldsSound	10.1007/BF03401797 doi (DE-627)SPR008057656 (SPR)BF03401797-e DE-627 ger DE-627 rakwb eng Goepfert, Christian verfasserin aut CD39 Modulates Endothelial Cell Activation and Apoptosis 2000 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Picower Institute Press 2000 Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. Human Umbilical Vein Endothelial Cells (HUVEC) (dpeaa)DE-He213 NTPDase Activity (dpeaa)DE-He213 Noninfected Cells (dpeaa)DE-He213 HUVEC Cultures (dpeaa)DE-He213 Infected HUVEC (dpeaa)DE-He213 Imai, Masato aut Brouard, Sophie aut Csizmadia, Eva aut Kaczmarek, Elzbieta aut Robson, Simon C. aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 6(2000), 7 vom: 01. Juli, Seite 591-603 (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:6 year:2000 number:7 day:01 month:07 pages:591-603 https://dx.doi.org/10.1007/BF03401797 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2875 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2000 7 01 07 591-603
language	English
source	Enthalten in Molecular medicine 6(2000), 7 vom: 01. Juli, Seite 591-603 volume:6 year:2000 number:7 day:01 month:07 pages:591-603
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The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. 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author	Goepfert, Christian
spellingShingle	Goepfert, Christian misc Human Umbilical Vein Endothelial Cells (HUVEC) misc NTPDase Activity misc Noninfected Cells misc HUVEC Cultures misc Infected HUVEC CD39 Modulates Endothelial Cell Activation and Apoptosis
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topic_title	CD39 Modulates Endothelial Cell Activation and Apoptosis Human Umbilical Vein Endothelial Cells (HUVEC) (dpeaa)DE-He213 NTPDase Activity (dpeaa)DE-He213 Noninfected Cells (dpeaa)DE-He213 HUVEC Cultures (dpeaa)DE-He213 Infected HUVEC (dpeaa)DE-He213
topic	misc Human Umbilical Vein Endothelial Cells (HUVEC) misc NTPDase Activity misc Noninfected Cells misc HUVEC Cultures misc Infected HUVEC
topic_unstemmed	misc Human Umbilical Vein Endothelial Cells (HUVEC) misc NTPDase Activity misc Noninfected Cells misc HUVEC Cultures misc Infected HUVEC
topic_browse	misc Human Umbilical Vein Endothelial Cells (HUVEC) misc NTPDase Activity misc Noninfected Cells misc HUVEC Cultures misc Infected HUVEC
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title	CD39 Modulates Endothelial Cell Activation and Apoptosis
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title_full	CD39 Modulates Endothelial Cell Activation and Apoptosis
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author_browse	Goepfert, Christian Imai, Masato Brouard, Sophie Csizmadia, Eva Kaczmarek, Elzbieta Robson, Simon C.
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title_sort	cd39 modulates endothelial cell activation and apoptosis
title_auth	CD39 Modulates Endothelial Cell Activation and Apoptosis
abstract	Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. © Picower Institute Press 2000
abstractGer	Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. © Picower Institute Press 2000
abstract_unstemmed	Background CD39 is the dominant vascular nucleoside triphosphate diphosphohydrolase (NTPDase) that exerts major effects on platelet reactivity by the regulated hydrolysis of extracellular adenine nucleotides. The effects of NTPDases on endothelial cell (EC) activation and apoptosis remain unexplored. Material and Methods Recombinant replication-deficient adenoviruses were constructed with human CD39 cDNA (rAdCD39) or the bacterial β-galactosidase (rAdβgal). Results Intact human umbilical vein EC cultures infected with rAdCD39 had substantial and stable increases in NTPDase biochemical activity (14.50 ± 3.50 Pi nmole/well/min), when contrasted with noninfected cells (0.95 ± 0.002) and rAdβgal infected cells (1.01 ± 0.02; p <0.005). Increased NTPDase activity efficiently inhibited immediate type 2Y purinergic receptor (P2Y)-mediated EC activation responses viz. von Willebrand factor secretion in response to extracellular ATP. In addition, CD39 up-regulation blocked ATP-induced translocation of the transcription nuclear factor (NF)-κB to the cell nucleus, and abrogated transcription of mRNA encoding E-selectin, and consequent protein synthesis. CD39 also decreased the extent of apoptosis triggered by putative type-2X purinergic (P2X7) receptors in response to high concentrations of extracellular ATP in vitro. Conclusion These properties of CD39 indicate primary vascular protective effects with potential therapeutic applications. © Picower Institute Press 2000
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title_short	CD39 Modulates Endothelial Cell Activation and Apoptosis
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author2	Imai, Masato Brouard, Sophie Csizmadia, Eva Kaczmarek, Elzbieta Robson, Simon C.
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CD39 Modulates Endothelial Cell Activation and Apoptosis

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