Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons
Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tis...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Lopachev, A. V. [verfasserIn] Lopacheva, O. M. [verfasserIn] Nikiforova, K. A. [verfasserIn] Filimonov, I. S. [verfasserIn] Fedorova, T. N. [verfasserIn] Akkuratov, E. E. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Biochemistry (Moscow) - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997, 83(2018), 2 vom: Feb., Seite 140-151 |
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| Übergeordnetes Werk: |
volume:83 ; year:2018 ; number:2 ; month:02 ; pages:140-151 |
| Links: |
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| DOI / URN: |
10.1134/S0006297918020062 |
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| Katalog-ID: |
SPR011024399 |
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| 245 | 1 | 0 | |a Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons |
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| 520 | |a Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. | ||
| 650 | 4 | |a cardiotonic steroids |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a digoxin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a bufalin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ouabain |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Na |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ,K |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a -ATPase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a primary cultures of neurons |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a toxicity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a MAP kinases |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ERK1/2 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a p38 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a JNK |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Lopacheva, O. M. |e verfasserin |4 aut | |
| 700 | 1 | |a Nikiforova, K. A. |e verfasserin |4 aut | |
| 700 | 1 | |a Filimonov, I. S. |e verfasserin |4 aut | |
| 700 | 1 | |a Fedorova, T. N. |e verfasserin |4 aut | |
| 700 | 1 | |a Akkuratov, E. E. |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Biochemistry (Moscow) |d Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 |g 83(2018), 2 vom: Feb., Seite 140-151 |w (DE-627)331746034 |w (DE-600)2052499-7 |x 1608-3040 |7 nnns |
| 773 | 1 | 8 | |g volume:83 |g year:2018 |g number:2 |g month:02 |g pages:140-151 |
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10.1134/S0006297918020062 doi (DE-627)SPR011024399 (SPR)S0006297918020062-e DE-627 ger DE-627 rakwb eng 540 ASE 35.70 bkl Lopachev, A. V. verfasserin aut Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. cardiotonic steroids (dpeaa)DE-He213 digoxin (dpeaa)DE-He213 bufalin (dpeaa)DE-He213 ouabain (dpeaa)DE-He213 Na (dpeaa)DE-He213 ,K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 primary cultures of neurons (dpeaa)DE-He213 toxicity (dpeaa)DE-He213 MAP kinases (dpeaa)DE-He213 ERK1/2 (dpeaa)DE-He213 p38 (dpeaa)DE-He213 JNK (dpeaa)DE-He213 Lopacheva, O. M. verfasserin aut Nikiforova, K. A. verfasserin aut Filimonov, I. S. verfasserin aut Fedorova, T. N. verfasserin aut Akkuratov, E. E. verfasserin aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 83(2018), 2 vom: Feb., Seite 140-151 (DE-627)331746034 (DE-600)2052499-7 1608-3040 nnns volume:83 year:2018 number:2 month:02 pages:140-151 https://dx.doi.org/10.1134/S0006297918020062 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_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_206 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_2056 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 35.70 ASE AR 83 2018 2 02 140-151 |
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10.1134/S0006297918020062 doi (DE-627)SPR011024399 (SPR)S0006297918020062-e DE-627 ger DE-627 rakwb eng 540 ASE 35.70 bkl Lopachev, A. V. verfasserin aut Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. cardiotonic steroids (dpeaa)DE-He213 digoxin (dpeaa)DE-He213 bufalin (dpeaa)DE-He213 ouabain (dpeaa)DE-He213 Na (dpeaa)DE-He213 ,K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 primary cultures of neurons (dpeaa)DE-He213 toxicity (dpeaa)DE-He213 MAP kinases (dpeaa)DE-He213 ERK1/2 (dpeaa)DE-He213 p38 (dpeaa)DE-He213 JNK (dpeaa)DE-He213 Lopacheva, O. M. verfasserin aut Nikiforova, K. A. verfasserin aut Filimonov, I. S. verfasserin aut Fedorova, T. N. verfasserin aut Akkuratov, E. E. verfasserin aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 83(2018), 2 vom: Feb., Seite 140-151 (DE-627)331746034 (DE-600)2052499-7 1608-3040 nnns volume:83 year:2018 number:2 month:02 pages:140-151 https://dx.doi.org/10.1134/S0006297918020062 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_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_206 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_2056 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 35.70 ASE AR 83 2018 2 02 140-151 |
| allfields_unstemmed |
10.1134/S0006297918020062 doi (DE-627)SPR011024399 (SPR)S0006297918020062-e DE-627 ger DE-627 rakwb eng 540 ASE 35.70 bkl Lopachev, A. V. verfasserin aut Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. cardiotonic steroids (dpeaa)DE-He213 digoxin (dpeaa)DE-He213 bufalin (dpeaa)DE-He213 ouabain (dpeaa)DE-He213 Na (dpeaa)DE-He213 ,K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 primary cultures of neurons (dpeaa)DE-He213 toxicity (dpeaa)DE-He213 MAP kinases (dpeaa)DE-He213 ERK1/2 (dpeaa)DE-He213 p38 (dpeaa)DE-He213 JNK (dpeaa)DE-He213 Lopacheva, O. M. verfasserin aut Nikiforova, K. A. verfasserin aut Filimonov, I. S. verfasserin aut Fedorova, T. N. verfasserin aut Akkuratov, E. E. verfasserin aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 83(2018), 2 vom: Feb., Seite 140-151 (DE-627)331746034 (DE-600)2052499-7 1608-3040 nnns volume:83 year:2018 number:2 month:02 pages:140-151 https://dx.doi.org/10.1134/S0006297918020062 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_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_206 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_2056 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 35.70 ASE AR 83 2018 2 02 140-151 |
| allfieldsGer |
10.1134/S0006297918020062 doi (DE-627)SPR011024399 (SPR)S0006297918020062-e DE-627 ger DE-627 rakwb eng 540 ASE 35.70 bkl Lopachev, A. V. verfasserin aut Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. cardiotonic steroids (dpeaa)DE-He213 digoxin (dpeaa)DE-He213 bufalin (dpeaa)DE-He213 ouabain (dpeaa)DE-He213 Na (dpeaa)DE-He213 ,K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 primary cultures of neurons (dpeaa)DE-He213 toxicity (dpeaa)DE-He213 MAP kinases (dpeaa)DE-He213 ERK1/2 (dpeaa)DE-He213 p38 (dpeaa)DE-He213 JNK (dpeaa)DE-He213 Lopacheva, O. M. verfasserin aut Nikiforova, K. A. verfasserin aut Filimonov, I. S. verfasserin aut Fedorova, T. N. verfasserin aut Akkuratov, E. E. verfasserin aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 83(2018), 2 vom: Feb., Seite 140-151 (DE-627)331746034 (DE-600)2052499-7 1608-3040 nnns volume:83 year:2018 number:2 month:02 pages:140-151 https://dx.doi.org/10.1134/S0006297918020062 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_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_206 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_2056 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 35.70 ASE AR 83 2018 2 02 140-151 |
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10.1134/S0006297918020062 doi (DE-627)SPR011024399 (SPR)S0006297918020062-e DE-627 ger DE-627 rakwb eng 540 ASE 35.70 bkl Lopachev, A. V. verfasserin aut Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. cardiotonic steroids (dpeaa)DE-He213 digoxin (dpeaa)DE-He213 bufalin (dpeaa)DE-He213 ouabain (dpeaa)DE-He213 Na (dpeaa)DE-He213 ,K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 primary cultures of neurons (dpeaa)DE-He213 toxicity (dpeaa)DE-He213 MAP kinases (dpeaa)DE-He213 ERK1/2 (dpeaa)DE-He213 p38 (dpeaa)DE-He213 JNK (dpeaa)DE-He213 Lopacheva, O. M. verfasserin aut Nikiforova, K. A. verfasserin aut Filimonov, I. S. verfasserin aut Fedorova, T. N. verfasserin aut Akkuratov, E. E. verfasserin aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 83(2018), 2 vom: Feb., Seite 140-151 (DE-627)331746034 (DE-600)2052499-7 1608-3040 nnns volume:83 year:2018 number:2 month:02 pages:140-151 https://dx.doi.org/10.1134/S0006297918020062 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_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_206 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_2056 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 35.70 ASE AR 83 2018 2 02 140-151 |
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Enthalten in Biochemistry (Moscow) 83(2018), 2 vom: Feb., Seite 140-151 volume:83 year:2018 number:2 month:02 pages:140-151 |
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Lopachev, A. V. @@aut@@ Lopacheva, O. M. @@aut@@ Nikiforova, K. A. @@aut@@ Filimonov, I. S. @@aut@@ Fedorova, T. N. @@aut@@ Akkuratov, E. E. @@aut@@ |
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| author |
Lopachev, A. V. |
| spellingShingle |
Lopachev, A. V. ddc 540 bkl 35.70 misc cardiotonic steroids misc digoxin misc bufalin misc ouabain misc Na misc ,K misc -ATPase misc primary cultures of neurons misc toxicity misc MAP kinases misc ERK1/2 misc p38 misc JNK Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons |
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| topic_title |
540 ASE 35.70 bkl Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons cardiotonic steroids (dpeaa)DE-He213 digoxin (dpeaa)DE-He213 bufalin (dpeaa)DE-He213 ouabain (dpeaa)DE-He213 Na (dpeaa)DE-He213 ,K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 primary cultures of neurons (dpeaa)DE-He213 toxicity (dpeaa)DE-He213 MAP kinases (dpeaa)DE-He213 ERK1/2 (dpeaa)DE-He213 p38 (dpeaa)DE-He213 JNK (dpeaa)DE-He213 |
| topic |
ddc 540 bkl 35.70 misc cardiotonic steroids misc digoxin misc bufalin misc ouabain misc Na misc ,K misc -ATPase misc primary cultures of neurons misc toxicity misc MAP kinases misc ERK1/2 misc p38 misc JNK |
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ddc 540 bkl 35.70 misc cardiotonic steroids misc digoxin misc bufalin misc ouabain misc Na misc ,K misc -ATPase misc primary cultures of neurons misc toxicity misc MAP kinases misc ERK1/2 misc p38 misc JNK |
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ddc 540 bkl 35.70 misc cardiotonic steroids misc digoxin misc bufalin misc ouabain misc Na misc ,K misc -ATPase misc primary cultures of neurons misc toxicity misc MAP kinases misc ERK1/2 misc p38 misc JNK |
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Biochemistry (Moscow) |
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Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons |
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Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons |
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Lopachev, A. V. |
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Biochemistry (Moscow) |
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Biochemistry (Moscow) |
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eng |
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Lopachev, A. V. Lopacheva, O. M. Nikiforova, K. A. Filimonov, I. S. Fedorova, T. N. Akkuratov, E. E. |
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540 ASE 35.70 bkl |
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Elektronische Aufsätze |
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Lopachev, A. V. |
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10.1134/S0006297918020062 |
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540 |
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verfasserin |
| title_sort |
comparative action of cardiotonic steroids on intracellular processes in rat cortical neurons |
| title_auth |
Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons |
| abstract |
Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. |
| abstractGer |
Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. |
| abstract_unstemmed |
Abstract Binding to $ Na^{+} $,$ K^{+} $-ATPase, cardiotonic steroids (CTS) activate intracellular signaling cascades that affect gene expression and regulation of proliferation and apoptosis in cells. Ouabain is the main CTS used for studying these processes. The effects of other CTS on nervous tissue are practically uncharacterized. Previously, we have shown that ouabain affects the activation of mitogen-activated protein kinases (MAP kinases) ERK1/2, p38, and JNK. In this study, we compared the effects of digoxin and bufalin, which belong to different subclasses of CTS, on primary culture of rat cortical cells. We found that CTS toxicity is not directly related to the degree of $ Na^{+} $,$ K^{+} $-ATPase inhibition, and that bufalin and digoxin, like ouabain, are capable of activating ERK1/2 and p38, but with different concentration and time profiles. Unlike bufalin and ouabain, digoxin did not decrease JNK activation after long-term incubation. We concluded that the toxic effect of CTS in concentrations that inhibit less than 80% of $ Na^{+} $,$ K^{+} $-ATPase activity is related to ERK1/2 activation as well as the complex profile of MAP kinase activation. A direct correlation between $ Na^{+} $,$ K^{+} $-ATPase inhibition and the degree of MAP kinase activation is only observed for ERK1/2. The different action of the three CTS on JNK and p38 activation may indicate that it is associated with intracellular signaling cascades triggered by protein–protein interactions between $ Na^{+} $,$ K^{+} $-ATPase and various partner proteins. Activation of MAP kinase pathways by these CTS occurs at concentrations that inhibit $ Na^{+} $,$ K^{+} $-ATPase containing the α1 subunit, suggesting that these signaling cascades are realized via α1. The results show that the signaling processes in neurons caused by CTS can differ not only because of different inhibitory constants for $ Na^{+} $,$ K^{+} $-ATPase. |
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Comparative Action of Cardiotonic Steroids on Intracellular Processes in Rat Cortical Neurons |
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https://dx.doi.org/10.1134/S0006297918020062 |
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Lopacheva, O. M. Nikiforova, K. A. Filimonov, I. S. Fedorova, T. N. Akkuratov, E. E. |
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Lopacheva, O. M. Nikiforova, K. A. Filimonov, I. S. Fedorova, T. N. Akkuratov, E. E. |
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10.1134/S0006297918020062 |
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2024-07-03T19:53:07.907Z |
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| score |
7.399541 |