Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model
Background The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hu, Jinwei [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Schlagwörter: |
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| Anmerkung: |
© Hu 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: Molecular cancer - London : Biomed Central, 2002, 6(2007), 1 vom: 14. März |
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| Übergeordnetes Werk: |
volume:6 ; year:2007 ; number:1 ; day:14 ; month:03 |
| Links: |
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| DOI / URN: |
10.1186/1476-4598-6-22 |
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| Katalog-ID: |
SPR028877098 |
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| 520 | |a Background The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. | ||
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| 700 | 1 | |a Yuan, Xiangpeng |4 aut | |
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| 700 | 1 | |a Sacapano, Manuel R |4 aut | |
| 700 | 1 | |a Wang, Xiao |4 aut | |
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| 700 | 1 | |a Espinoza, Andres |4 aut | |
| 700 | 1 | |a Prosolovich, Ksenia |4 aut | |
| 700 | 1 | |a Ong, John M |4 aut | |
| 700 | 1 | |a Irvin, Dwain |4 aut | |
| 700 | 1 | |a Black, Keith L |4 aut | |
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10.1186/1476-4598-6-22 doi (DE-627)SPR028877098 (SPR)1476-4598-6-22-e DE-627 ger DE-627 rakwb eng Hu, Jinwei verfasserin aut Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. Brain Tumor (dpeaa)DE-He213 Brain Metastasis (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 Primary Brain Tumor (dpeaa)DE-He213 Normal Brain Tissue (dpeaa)DE-He213 Yuan, Xiangpeng aut Ko, MinHee K aut Yin, Dali aut Sacapano, Manuel R aut Wang, Xiao aut Konda, Bindu M aut Espinoza, Andres aut Prosolovich, Ksenia aut Ong, John M aut Irvin, Dwain aut Black, Keith L aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 14. März (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:14 month:03 https://dx.doi.org/10.1186/1476-4598-6-22 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_70 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 6 2007 1 14 03 |
| spelling |
10.1186/1476-4598-6-22 doi (DE-627)SPR028877098 (SPR)1476-4598-6-22-e DE-627 ger DE-627 rakwb eng Hu, Jinwei verfasserin aut Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. Brain Tumor (dpeaa)DE-He213 Brain Metastasis (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 Primary Brain Tumor (dpeaa)DE-He213 Normal Brain Tissue (dpeaa)DE-He213 Yuan, Xiangpeng aut Ko, MinHee K aut Yin, Dali aut Sacapano, Manuel R aut Wang, Xiao aut Konda, Bindu M aut Espinoza, Andres aut Prosolovich, Ksenia aut Ong, John M aut Irvin, Dwain aut Black, Keith L aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 14. März (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:14 month:03 https://dx.doi.org/10.1186/1476-4598-6-22 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_70 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 6 2007 1 14 03 |
| allfields_unstemmed |
10.1186/1476-4598-6-22 doi (DE-627)SPR028877098 (SPR)1476-4598-6-22-e DE-627 ger DE-627 rakwb eng Hu, Jinwei verfasserin aut Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. Brain Tumor (dpeaa)DE-He213 Brain Metastasis (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 Primary Brain Tumor (dpeaa)DE-He213 Normal Brain Tissue (dpeaa)DE-He213 Yuan, Xiangpeng aut Ko, MinHee K aut Yin, Dali aut Sacapano, Manuel R aut Wang, Xiao aut Konda, Bindu M aut Espinoza, Andres aut Prosolovich, Ksenia aut Ong, John M aut Irvin, Dwain aut Black, Keith L aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 14. März (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:14 month:03 https://dx.doi.org/10.1186/1476-4598-6-22 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_70 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 6 2007 1 14 03 |
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10.1186/1476-4598-6-22 doi (DE-627)SPR028877098 (SPR)1476-4598-6-22-e DE-627 ger DE-627 rakwb eng Hu, Jinwei verfasserin aut Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. Brain Tumor (dpeaa)DE-He213 Brain Metastasis (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 Primary Brain Tumor (dpeaa)DE-He213 Normal Brain Tissue (dpeaa)DE-He213 Yuan, Xiangpeng aut Ko, MinHee K aut Yin, Dali aut Sacapano, Manuel R aut Wang, Xiao aut Konda, Bindu M aut Espinoza, Andres aut Prosolovich, Ksenia aut Ong, John M aut Irvin, Dwain aut Black, Keith L aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 14. März (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:14 month:03 https://dx.doi.org/10.1186/1476-4598-6-22 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_70 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 6 2007 1 14 03 |
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10.1186/1476-4598-6-22 doi (DE-627)SPR028877098 (SPR)1476-4598-6-22-e DE-627 ger DE-627 rakwb eng Hu, Jinwei verfasserin aut Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. Brain Tumor (dpeaa)DE-He213 Brain Metastasis (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 Primary Brain Tumor (dpeaa)DE-He213 Normal Brain Tissue (dpeaa)DE-He213 Yuan, Xiangpeng aut Ko, MinHee K aut Yin, Dali aut Sacapano, Manuel R aut Wang, Xiao aut Konda, Bindu M aut Espinoza, Andres aut Prosolovich, Ksenia aut Ong, John M aut Irvin, Dwain aut Black, Keith L aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 14. März (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:14 month:03 https://dx.doi.org/10.1186/1476-4598-6-22 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_70 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 6 2007 1 14 03 |
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Hu, Jinwei @@aut@@ Yuan, Xiangpeng @@aut@@ Ko, MinHee K @@aut@@ Yin, Dali @@aut@@ Sacapano, Manuel R @@aut@@ Wang, Xiao @@aut@@ Konda, Bindu M @@aut@@ Espinoza, Andres @@aut@@ Prosolovich, Ksenia @@aut@@ Ong, John M @@aut@@ Irvin, Dwain @@aut@@ Black, Keith L @@aut@@ |
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Hu, Jinwei Yuan, Xiangpeng Ko, MinHee K Yin, Dali Sacapano, Manuel R Wang, Xiao Konda, Bindu M Espinoza, Andres Prosolovich, Ksenia Ong, John M Irvin, Dwain Black, Keith L |
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calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model |
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Calcium-activated potassium channels mediated blood-brain tumor barrier opening in a rat metastatic brain tumor model |
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Background The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. © Hu 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 The blood-brain tumor barrier (BTB) impedes the delivery of therapeutic agents to brain tumors. While adequate delivery of drugs occurs in systemic tumors, the BTB limits delivery of anti-tumor agents into brain metastases. Results In this study, we examined the function and regulation of calcium-activated potassium ($ K_{Ca} $) channels in a rat metastatic brain tumor model. We showed that intravenous infusion of NS1619, a $ K_{Ca} $ channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain. Iberiotoxin, a $ K_{Ca} $ channel antagonist, significantly attenuated NS1619-induced BTB permeability increase. We found $ K_{Ca} $ channels and bradykinin type 2 receptors (B2R) expressed in cultured human metastatic brain tumor cells (CRL-5904, non-small cell lung cancer, metastasized to brain), human brain microvessel endothelial cells (HBMEC) and human lung cancer brain metastasis tissues. Potentiometric assays demonstrated the activity of $ K_{Ca} $ channels in metastatic brain tumor cells and HBMEC. Furthermore, we detected higher expression of $ K_{Ca} $ channels in the metastatic brain tumor tissue and tumor capillary endothelia as compared to normal brain tissue. Co-culture of metastatic brain tumor cells and brain microvessel endothelial cells showed an upregulation of $ K_{Ca} $ channels, which may contribute to the overexpression of $ K_{Ca} $ channels in tumor microvessels and selectivity of BTB opening. Conclusion These findings suggest that $ K_{Ca} $ channels in metastatic brain tumors may serve as an effective target for biochemical modulation of BTB permeability to enhance selective delivery of chemotherapeutic drugs to metastatic brain tumors. © Hu 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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| score |
7.398695 |