Activated protein C and thrombin participate in the regulation of astrocyte functions
Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ivanova, A. E. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014 |
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| Schlagwörter: |
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| Anmerkung: |
© Pleiades Publishing, Ltd. 2014 |
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| Übergeordnetes Werk: |
Enthalten in: Biochemistry (Moscow) - Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007, 8(2014), 1 vom: Jan., Seite 50-59 |
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| Übergeordnetes Werk: |
volume:8 ; year:2014 ; number:1 ; month:01 ; pages:50-59 |
| Links: |
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| DOI / URN: |
10.1134/S1990747813050048 |
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| Katalog-ID: |
SPR02259423X |
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| 100 | 1 | |a Ivanova, A. E. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Activated protein C and thrombin participate in the regulation of astrocyte functions |
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| 520 | |a Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. | ||
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| 700 | 1 | |a Gorbacheva, L. R. |4 aut | |
| 700 | 1 | |a Strukova, S. M. |4 aut | |
| 700 | 1 | |a Pinelis, V. G. |4 aut | |
| 700 | 1 | |a Reiser, G. |4 aut | |
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10.1134/S1990747813050048 doi (DE-627)SPR02259423X (SPR)S1990747813050048-e DE-627 ger DE-627 rakwb eng Ivanova, A. E. verfasserin aut Activated protein C and thrombin participate in the regulation of astrocyte functions 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2014 Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. astrogliosis (dpeaa)DE-He213 thrombin (dpeaa)DE-He213 activated protein C (APC) (dpeaa)DE-He213 stress fibrils (dpeaa)DE-He213 S100b (dpeaa)DE-He213 “free fields” (dpeaa)DE-He213 Gorbacheva, L. R. aut Strukova, S. M. aut Pinelis, V. G. aut Reiser, G. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 8(2014), 1 vom: Jan., Seite 50-59 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:8 year:2014 number:1 month:01 pages:50-59 https://dx.doi.org/10.1134/S1990747813050048 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 8 2014 1 01 50-59 |
| spelling |
10.1134/S1990747813050048 doi (DE-627)SPR02259423X (SPR)S1990747813050048-e DE-627 ger DE-627 rakwb eng Ivanova, A. E. verfasserin aut Activated protein C and thrombin participate in the regulation of astrocyte functions 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2014 Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. astrogliosis (dpeaa)DE-He213 thrombin (dpeaa)DE-He213 activated protein C (APC) (dpeaa)DE-He213 stress fibrils (dpeaa)DE-He213 S100b (dpeaa)DE-He213 “free fields” (dpeaa)DE-He213 Gorbacheva, L. R. aut Strukova, S. M. aut Pinelis, V. G. aut Reiser, G. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 8(2014), 1 vom: Jan., Seite 50-59 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:8 year:2014 number:1 month:01 pages:50-59 https://dx.doi.org/10.1134/S1990747813050048 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 8 2014 1 01 50-59 |
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10.1134/S1990747813050048 doi (DE-627)SPR02259423X (SPR)S1990747813050048-e DE-627 ger DE-627 rakwb eng Ivanova, A. E. verfasserin aut Activated protein C and thrombin participate in the regulation of astrocyte functions 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2014 Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. astrogliosis (dpeaa)DE-He213 thrombin (dpeaa)DE-He213 activated protein C (APC) (dpeaa)DE-He213 stress fibrils (dpeaa)DE-He213 S100b (dpeaa)DE-He213 “free fields” (dpeaa)DE-He213 Gorbacheva, L. R. aut Strukova, S. M. aut Pinelis, V. G. aut Reiser, G. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 8(2014), 1 vom: Jan., Seite 50-59 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:8 year:2014 number:1 month:01 pages:50-59 https://dx.doi.org/10.1134/S1990747813050048 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 8 2014 1 01 50-59 |
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10.1134/S1990747813050048 doi (DE-627)SPR02259423X (SPR)S1990747813050048-e DE-627 ger DE-627 rakwb eng Ivanova, A. E. verfasserin aut Activated protein C and thrombin participate in the regulation of astrocyte functions 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2014 Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. astrogliosis (dpeaa)DE-He213 thrombin (dpeaa)DE-He213 activated protein C (APC) (dpeaa)DE-He213 stress fibrils (dpeaa)DE-He213 S100b (dpeaa)DE-He213 “free fields” (dpeaa)DE-He213 Gorbacheva, L. R. aut Strukova, S. M. aut Pinelis, V. G. aut Reiser, G. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 8(2014), 1 vom: Jan., Seite 50-59 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:8 year:2014 number:1 month:01 pages:50-59 https://dx.doi.org/10.1134/S1990747813050048 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 8 2014 1 01 50-59 |
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10.1134/S1990747813050048 doi (DE-627)SPR02259423X (SPR)S1990747813050048-e DE-627 ger DE-627 rakwb eng Ivanova, A. E. verfasserin aut Activated protein C and thrombin participate in the regulation of astrocyte functions 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2014 Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. astrogliosis (dpeaa)DE-He213 thrombin (dpeaa)DE-He213 activated protein C (APC) (dpeaa)DE-He213 stress fibrils (dpeaa)DE-He213 S100b (dpeaa)DE-He213 “free fields” (dpeaa)DE-He213 Gorbacheva, L. R. aut Strukova, S. M. aut Pinelis, V. G. aut Reiser, G. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 8(2014), 1 vom: Jan., Seite 50-59 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:8 year:2014 number:1 month:01 pages:50-59 https://dx.doi.org/10.1134/S1990747813050048 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 8 2014 1 01 50-59 |
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English |
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Enthalten in Biochemistry (Moscow) 8(2014), 1 vom: Jan., Seite 50-59 volume:8 year:2014 number:1 month:01 pages:50-59 |
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Enthalten in Biochemistry (Moscow) 8(2014), 1 vom: Jan., Seite 50-59 volume:8 year:2014 number:1 month:01 pages:50-59 |
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Ivanova, A. E. @@aut@@ Gorbacheva, L. R. @@aut@@ Strukova, S. M. @@aut@@ Pinelis, V. G. @@aut@@ Reiser, G. @@aut@@ |
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In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. 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Ivanova, A. E. |
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Ivanova, A. E. misc astrogliosis misc thrombin misc activated protein C (APC) misc stress fibrils misc S100b misc “free fields” Activated protein C and thrombin participate in the regulation of astrocyte functions |
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Activated protein C and thrombin participate in the regulation of astrocyte functions astrogliosis (dpeaa)DE-He213 thrombin (dpeaa)DE-He213 activated protein C (APC) (dpeaa)DE-He213 stress fibrils (dpeaa)DE-He213 S100b (dpeaa)DE-He213 “free fields” (dpeaa)DE-He213 |
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misc astrogliosis misc thrombin misc activated protein C (APC) misc stress fibrils misc S100b misc “free fields” |
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misc astrogliosis misc thrombin misc activated protein C (APC) misc stress fibrils misc S100b misc “free fields” |
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Activated protein C and thrombin participate in the regulation of astrocyte functions |
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Ivanova, A. E. |
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Ivanova, A. E. Gorbacheva, L. R. Strukova, S. M. Pinelis, V. G. Reiser, G. |
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activated protein c and thrombin participate in the regulation of astrocyte functions |
| title_auth |
Activated protein C and thrombin participate in the regulation of astrocyte functions |
| abstract |
Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. © Pleiades Publishing, Ltd. 2014 |
| abstractGer |
Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. © Pleiades Publishing, Ltd. 2014 |
| abstract_unstemmed |
Abstract Protein C anticoagulant system is a multifunctional cofactor-dependent system. In addition to anticoagulant function, activated protein C (APC) also exhibits neuroprotective activity in hypoxia and stroke, but there are no data on potential effects of APC on astrocytes. In the present work we have studied the influence of APC and thrombin on rat astrocytes in primary culture. It was found that thrombin at concentrations above 10 nM (1 U/mL) induced significant activation in the cultured astrocytes resulting in reactive astrogliosis. The cultures exposed to thrombin for 24 h demonstrated a significant increase in proliferation and the S100b protein expression. Thrombin at high concentrations produced visible changes in the cytoskeleton of astrocytes, in particular, an increase in the number of stress fibers in the cultured cells. Moreover, thrombin apparently affected astrocyte migration. Thus, the treatment of serum-starved astrocytes with thrombin resulted in changes in cell monolayer uniformity and formation of “free fields”. APC prevented thrombin-induced proliferation of astrocytes and the S100b protein expression, reducing the parameters under study to the control values. In addition, APC reduced thrombin-induced disorganization of fibrils and formation of “free fields”. The results have demonstrated a new aspect of the protective effect of APC, which suppresses astrocyte activation induced by the proinflammatory effect of thrombin. It suggests a potential application of APC as a regulator of astrogliosis in pathological brain conditions. © Pleiades Publishing, Ltd. 2014 |
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Activated protein C and thrombin participate in the regulation of astrocyte functions |
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https://dx.doi.org/10.1134/S1990747813050048 |
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Gorbacheva, L. R. Strukova, S. M. Pinelis, V. G. Reiser, G. |
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Gorbacheva, L. R. Strukova, S. M. Pinelis, V. G. Reiser, G. |
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2024-07-03T13:54:09.699Z |
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| score |
7.4014435 |