Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons
Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective eff...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Serchov, Tsvetan [verfasserIn] Atas, Hasan-Cem [verfasserIn] Normann, Claus [verfasserIn] van Calker, Dietrich [verfasserIn] Biber, Knut [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Molecular neurobiology - Totowa, NJ : Humana Press, 1987, 46(2012), 2 vom: 17. Aug., Seite 535-544 |
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| Übergeordnetes Werk: |
volume:46 ; year:2012 ; number:2 ; day:17 ; month:08 ; pages:535-544 |
| Links: |
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| DOI / URN: |
10.1007/s12035-012-8321-6 |
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| Katalog-ID: |
SPR023951907 |
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| 520 | |a Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. | ||
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| 650 | 4 | |a Neuroprotection |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Tetracycline expression system |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Normann, Claus |e verfasserin |4 aut | |
| 700 | 1 | |a van Calker, Dietrich |e verfasserin |4 aut | |
| 700 | 1 | |a Biber, Knut |e verfasserin |4 aut | |
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10.1007/s12035-012-8321-6 doi (DE-627)SPR023951907 (SPR)s12035-012-8321-6-e DE-627 ger DE-627 rakwb eng 610 570 ASE 44.90 bkl Serchov, Tsvetan verfasserin aut Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. Adenosine A (dpeaa)DE-He213 receptor (dpeaa)DE-He213 Overexpression (dpeaa)DE-He213 Excitotoxicity (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 Tetracycline expression system (dpeaa)DE-He213 Transfection (dpeaa)DE-He213 Atas, Hasan-Cem verfasserin aut Normann, Claus verfasserin aut van Calker, Dietrich verfasserin aut Biber, Knut verfasserin aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 46(2012), 2 vom: 17. Aug., Seite 535-544 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:46 year:2012 number:2 day:17 month:08 pages:535-544 https://dx.doi.org/10.1007/s12035-012-8321-6 lizenzpflichtig 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_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 46 2012 2 17 08 535-544 |
| spelling |
10.1007/s12035-012-8321-6 doi (DE-627)SPR023951907 (SPR)s12035-012-8321-6-e DE-627 ger DE-627 rakwb eng 610 570 ASE 44.90 bkl Serchov, Tsvetan verfasserin aut Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. Adenosine A (dpeaa)DE-He213 receptor (dpeaa)DE-He213 Overexpression (dpeaa)DE-He213 Excitotoxicity (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 Tetracycline expression system (dpeaa)DE-He213 Transfection (dpeaa)DE-He213 Atas, Hasan-Cem verfasserin aut Normann, Claus verfasserin aut van Calker, Dietrich verfasserin aut Biber, Knut verfasserin aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 46(2012), 2 vom: 17. Aug., Seite 535-544 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:46 year:2012 number:2 day:17 month:08 pages:535-544 https://dx.doi.org/10.1007/s12035-012-8321-6 lizenzpflichtig 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_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 46 2012 2 17 08 535-544 |
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10.1007/s12035-012-8321-6 doi (DE-627)SPR023951907 (SPR)s12035-012-8321-6-e DE-627 ger DE-627 rakwb eng 610 570 ASE 44.90 bkl Serchov, Tsvetan verfasserin aut Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. Adenosine A (dpeaa)DE-He213 receptor (dpeaa)DE-He213 Overexpression (dpeaa)DE-He213 Excitotoxicity (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 Tetracycline expression system (dpeaa)DE-He213 Transfection (dpeaa)DE-He213 Atas, Hasan-Cem verfasserin aut Normann, Claus verfasserin aut van Calker, Dietrich verfasserin aut Biber, Knut verfasserin aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 46(2012), 2 vom: 17. Aug., Seite 535-544 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:46 year:2012 number:2 day:17 month:08 pages:535-544 https://dx.doi.org/10.1007/s12035-012-8321-6 lizenzpflichtig 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_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 46 2012 2 17 08 535-544 |
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10.1007/s12035-012-8321-6 doi (DE-627)SPR023951907 (SPR)s12035-012-8321-6-e DE-627 ger DE-627 rakwb eng 610 570 ASE 44.90 bkl Serchov, Tsvetan verfasserin aut Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. Adenosine A (dpeaa)DE-He213 receptor (dpeaa)DE-He213 Overexpression (dpeaa)DE-He213 Excitotoxicity (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 Tetracycline expression system (dpeaa)DE-He213 Transfection (dpeaa)DE-He213 Atas, Hasan-Cem verfasserin aut Normann, Claus verfasserin aut van Calker, Dietrich verfasserin aut Biber, Knut verfasserin aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 46(2012), 2 vom: 17. Aug., Seite 535-544 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:46 year:2012 number:2 day:17 month:08 pages:535-544 https://dx.doi.org/10.1007/s12035-012-8321-6 lizenzpflichtig 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_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 46 2012 2 17 08 535-544 |
| allfieldsSound |
10.1007/s12035-012-8321-6 doi (DE-627)SPR023951907 (SPR)s12035-012-8321-6-e DE-627 ger DE-627 rakwb eng 610 570 ASE 44.90 bkl Serchov, Tsvetan verfasserin aut Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. Adenosine A (dpeaa)DE-He213 receptor (dpeaa)DE-He213 Overexpression (dpeaa)DE-He213 Excitotoxicity (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 Tetracycline expression system (dpeaa)DE-He213 Transfection (dpeaa)DE-He213 Atas, Hasan-Cem verfasserin aut Normann, Claus verfasserin aut van Calker, Dietrich verfasserin aut Biber, Knut verfasserin aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 46(2012), 2 vom: 17. Aug., Seite 535-544 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:46 year:2012 number:2 day:17 month:08 pages:535-544 https://dx.doi.org/10.1007/s12035-012-8321-6 lizenzpflichtig 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_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 46 2012 2 17 08 535-544 |
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Enthalten in Molecular neurobiology 46(2012), 2 vom: 17. Aug., Seite 535-544 volume:46 year:2012 number:2 day:17 month:08 pages:535-544 |
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Enthalten in Molecular neurobiology 46(2012), 2 vom: 17. Aug., Seite 535-544 volume:46 year:2012 number:2 day:17 month:08 pages:535-544 |
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Adenosine A receptor Overexpression Excitotoxicity Neuroprotection Tetracycline expression system Transfection |
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Molecular neurobiology |
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Serchov, Tsvetan @@aut@@ Atas, Hasan-Cem @@aut@@ Normann, Claus @@aut@@ van Calker, Dietrich @@aut@@ Biber, Knut @@aut@@ |
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2012-08-17T00:00:00Z |
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This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. 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Serchov, Tsvetan |
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Serchov, Tsvetan ddc 610 bkl 44.90 misc Adenosine A misc receptor misc Overexpression misc Excitotoxicity misc Neuroprotection misc Tetracycline expression system misc Transfection Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons |
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610 570 ASE 44.90 bkl Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons Adenosine A (dpeaa)DE-He213 receptor (dpeaa)DE-He213 Overexpression (dpeaa)DE-He213 Excitotoxicity (dpeaa)DE-He213 Neuroprotection (dpeaa)DE-He213 Tetracycline expression system (dpeaa)DE-He213 Transfection (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc Adenosine A misc receptor misc Overexpression misc Excitotoxicity misc Neuroprotection misc Tetracycline expression system misc Transfection |
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genetically controlled upregulation of adenosine $ a_{1} $ receptor expression enhances the survival of primary cortical neurons |
| title_auth |
Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons |
| abstract |
Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. |
| abstractGer |
Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. |
| abstract_unstemmed |
Abstract Adenosine has a key endogenous neuroprotective role in the brain, predominantly mediated by the adenosine $ A_{1} $ receptor ($ A_{1} $R). This has been mainly explored using pharmacological tools and/or receptor knockout mice strains. It has long been suggested that the neuroprotective effects of $ A_{1} $R are increased following receptor upregulation, thus attenuating neuronal damage in pathological conditions. We have previously shown that the neuroprotective and neuromodulatory actions of the cytokines IL-6 and oncostatin M are mediated by induction of neuronal $ A_{1} $R expression. In order to investigate the direct effects of $ A_{1} $R upregulation in neurons, we have generated a tetracycline-regulated expression system with a bidirectional promoter, directing the simultaneous expression of the mouse $ A_{1} $R and GFP/mCherry reporter genes. In a first step, we tested the efficacy of the system in transiently transfected human embryonic kidney 293 cells. In addition, we confirmed the functional integrity of the expressed $ A_{1} $R by whole-cell patch clamp recordings. We demonstrated that $ A_{1} $R-transfected primary neurons show enhanced survival against N-methyl-d-aspartate-induced excitotoxicity. Pretreatment with an $ A_{1} $R-selective agonist additionally strongly decreased neuronal cell death, while an $ A_{1} $R antagonist completely abolished the neuroprotective effects of $ A_{1} $R upregulation. The presented data provide for the first time direct evidence that the upregulation of $ A_{1} $R enhances neuronal survival. |
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Genetically Controlled Upregulation of Adenosine $ A_{1} $ Receptor Expression Enhances the Survival of Primary Cortical Neurons |
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| score |
7.399107 |