Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells
Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (C...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Shelby, Bryan D [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Schlagwörter: |
Endothelial Cell Growth Supplement |
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| Anmerkung: |
© Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: Virology journal - London : BioMed Central, 2004, 4(2007), 1 vom: 14. Sept. |
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| Übergeordnetes Werk: |
volume:4 ; year:2007 ; number:1 ; day:14 ; month:09 |
| Links: |
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| DOI / URN: |
10.1186/1743-422X-4-87 |
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| Katalog-ID: |
SPR029234344 |
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| 520 | |a Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. | ||
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| 700 | 1 | |a Offermann, Margaret K |4 aut | |
| 700 | 1 | |a Morris, Cindy A |4 aut | |
| 700 | 1 | |a Sullivan, Deborah E |4 aut | |
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10.1186/1743-422X-4-87 doi (DE-627)SPR029234344 (SPR)1743-422X-4-87-e DE-627 ger DE-627 rakwb eng Shelby, Bryan D verfasserin aut Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. Endothelial Cell Growth Supplement (dpeaa)DE-He213 Human Umbilical Vascular Endothelial Cell (dpeaa)DE-He213 PGE2 Secretion (dpeaa)DE-He213 KSHV Gene (dpeaa)DE-He213 KSHV Replication (dpeaa)DE-He213 LaMarca, Heather L aut McFerrin, Harris E aut Nelson, Anne B aut Lasky, Joseph A aut Sun, Gang aut Myatt, Leslie aut Offermann, Margaret K aut Morris, Cindy A aut Sullivan, Deborah E aut Enthalten in Virology journal London : BioMed Central, 2004 4(2007), 1 vom: 14. Sept. (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:4 year:2007 number:1 day:14 month:09 https://dx.doi.org/10.1186/1743-422X-4-87 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 4 2007 1 14 09 |
| spelling |
10.1186/1743-422X-4-87 doi (DE-627)SPR029234344 (SPR)1743-422X-4-87-e DE-627 ger DE-627 rakwb eng Shelby, Bryan D verfasserin aut Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. Endothelial Cell Growth Supplement (dpeaa)DE-He213 Human Umbilical Vascular Endothelial Cell (dpeaa)DE-He213 PGE2 Secretion (dpeaa)DE-He213 KSHV Gene (dpeaa)DE-He213 KSHV Replication (dpeaa)DE-He213 LaMarca, Heather L aut McFerrin, Harris E aut Nelson, Anne B aut Lasky, Joseph A aut Sun, Gang aut Myatt, Leslie aut Offermann, Margaret K aut Morris, Cindy A aut Sullivan, Deborah E aut Enthalten in Virology journal London : BioMed Central, 2004 4(2007), 1 vom: 14. Sept. (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:4 year:2007 number:1 day:14 month:09 https://dx.doi.org/10.1186/1743-422X-4-87 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 4 2007 1 14 09 |
| allfields_unstemmed |
10.1186/1743-422X-4-87 doi (DE-627)SPR029234344 (SPR)1743-422X-4-87-e DE-627 ger DE-627 rakwb eng Shelby, Bryan D verfasserin aut Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. Endothelial Cell Growth Supplement (dpeaa)DE-He213 Human Umbilical Vascular Endothelial Cell (dpeaa)DE-He213 PGE2 Secretion (dpeaa)DE-He213 KSHV Gene (dpeaa)DE-He213 KSHV Replication (dpeaa)DE-He213 LaMarca, Heather L aut McFerrin, Harris E aut Nelson, Anne B aut Lasky, Joseph A aut Sun, Gang aut Myatt, Leslie aut Offermann, Margaret K aut Morris, Cindy A aut Sullivan, Deborah E aut Enthalten in Virology journal London : BioMed Central, 2004 4(2007), 1 vom: 14. Sept. (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:4 year:2007 number:1 day:14 month:09 https://dx.doi.org/10.1186/1743-422X-4-87 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 4 2007 1 14 09 |
| allfieldsGer |
10.1186/1743-422X-4-87 doi (DE-627)SPR029234344 (SPR)1743-422X-4-87-e DE-627 ger DE-627 rakwb eng Shelby, Bryan D verfasserin aut Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. Endothelial Cell Growth Supplement (dpeaa)DE-He213 Human Umbilical Vascular Endothelial Cell (dpeaa)DE-He213 PGE2 Secretion (dpeaa)DE-He213 KSHV Gene (dpeaa)DE-He213 KSHV Replication (dpeaa)DE-He213 LaMarca, Heather L aut McFerrin, Harris E aut Nelson, Anne B aut Lasky, Joseph A aut Sun, Gang aut Myatt, Leslie aut Offermann, Margaret K aut Morris, Cindy A aut Sullivan, Deborah E aut Enthalten in Virology journal London : BioMed Central, 2004 4(2007), 1 vom: 14. Sept. (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:4 year:2007 number:1 day:14 month:09 https://dx.doi.org/10.1186/1743-422X-4-87 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 4 2007 1 14 09 |
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10.1186/1743-422X-4-87 doi (DE-627)SPR029234344 (SPR)1743-422X-4-87-e DE-627 ger DE-627 rakwb eng Shelby, Bryan D verfasserin aut Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. Endothelial Cell Growth Supplement (dpeaa)DE-He213 Human Umbilical Vascular Endothelial Cell (dpeaa)DE-He213 PGE2 Secretion (dpeaa)DE-He213 KSHV Gene (dpeaa)DE-He213 KSHV Replication (dpeaa)DE-He213 LaMarca, Heather L aut McFerrin, Harris E aut Nelson, Anne B aut Lasky, Joseph A aut Sun, Gang aut Myatt, Leslie aut Offermann, Margaret K aut Morris, Cindy A aut Sullivan, Deborah E aut Enthalten in Virology journal London : BioMed Central, 2004 4(2007), 1 vom: 14. Sept. (DE-627)394165004 (DE-600)2160640-7 1743-422X nnns volume:4 year:2007 number:1 day:14 month:09 https://dx.doi.org/10.1186/1743-422X-4-87 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 4 2007 1 14 09 |
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Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells |
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Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells |
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Shelby, Bryan D LaMarca, Heather L McFerrin, Harris E Nelson, Anne B Lasky, Joseph A Sun, Gang Myatt, Leslie Offermann, Margaret K Morris, Cindy A Sullivan, Deborah E |
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10.1186/1743-422X-4-87 |
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kaposi's sarcoma associated herpesvirus g-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells |
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Kaposi's sarcoma associated herpesvirus G-protein coupled receptor activation of cyclooxygenase-2 in vascular endothelial cells |
| abstract |
Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Background Kaposi's sarcoma associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a highly vascularized neoplasm characterized by endothelial-derived spindle-shaped tumor cells. KSHV-infected microvascular endothelial cells demonstrate increased cyclooxygenase-2 (COX-2) expression and KS lesions have high levels of prostaglandin $ E_{2} $ ($ PGE_{2} $), a short-lived eicosanoid dependent on cyclooxygenase activity that has been linked to pathogenesis of other neoplasias. To determine whether increased COX-2 expression and $ PGE_{2} $ production is mediated by the angiogenic and tumorigenic KSHV-encoded G-protein coupled receptor (vGPCR), we developed a recombinant retrovirus to express vGPCR in Human Umbilical Vascular Endothelial Cells (HUVEC). Results In the present study, we show that vGPCR-expressing HUVEC exhibit a spindle-like morphology that is characteristic of KS endothelial cells and demonstrate selective induction of $ PGE_{2} $ and COX-2. By treating vGPCR-expressing HUVEC with selective and non-selective COX inhibitors, we show that vGPCR-induced $ PGE_{2} $ production is dependent on the expression of COX-2 but not COX-1. Conclusion Taken together, these results demonstrate that vGPCR induces expression of COX-2 and $ PGE_{2} $ that may mediate the paracrine effects of this key viral protein in KS pathogenesis. © Shelby et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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