Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice
Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs)...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Maeda, Yuki [verfasserIn] Motoyama, Keiichi [verfasserIn] Higashi, Taishi [verfasserIn] Onodera, Risako [verfasserIn] Takeo, Toru [verfasserIn] Nakagata, Naomi [verfasserIn] Kurauchi, Yuki [verfasserIn] Katsuki, Hiroshi [verfasserIn] Ishitsuka, Yoichi [verfasserIn] Kondo, Yuki [verfasserIn] Irie, Tetsumi [verfasserIn] Era, Takumi [verfasserIn] Arima, Hidetoshi [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: Journal of inclusion phenomena and macrocyclic chemistry - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983, 93(2018), 1-2 vom: 21. Aug., Seite 53-66 |
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| Übergeordnetes Werk: |
volume:93 ; year:2018 ; number:1-2 ; day:21 ; month:08 ; pages:53-66 |
| Links: |
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| DOI / URN: |
10.1007/s10847-018-0835-8 |
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| Katalog-ID: |
SPR013727907 |
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| 100 | 1 | |a Maeda, Yuki |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
| 264 | 1 | |c 2018 | |
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| 520 | |a Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. | ||
| 650 | 4 | |a Cyclodextrins |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a GM1-gangliosidosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a GM1-ganglioside, cholesterol, lysosomes |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Motoyama, Keiichi |e verfasserin |4 aut | |
| 700 | 1 | |a Higashi, Taishi |e verfasserin |4 aut | |
| 700 | 1 | |a Onodera, Risako |e verfasserin |4 aut | |
| 700 | 1 | |a Takeo, Toru |e verfasserin |4 aut | |
| 700 | 1 | |a Nakagata, Naomi |e verfasserin |4 aut | |
| 700 | 1 | |a Kurauchi, Yuki |e verfasserin |4 aut | |
| 700 | 1 | |a Katsuki, Hiroshi |e verfasserin |4 aut | |
| 700 | 1 | |a Ishitsuka, Yoichi |e verfasserin |4 aut | |
| 700 | 1 | |a Kondo, Yuki |e verfasserin |4 aut | |
| 700 | 1 | |a Irie, Tetsumi |e verfasserin |4 aut | |
| 700 | 1 | |a Era, Takumi |e verfasserin |4 aut | |
| 700 | 1 | |a Arima, Hidetoshi |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of inclusion phenomena and macrocyclic chemistry |d Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 |g 93(2018), 1-2 vom: 21. Aug., Seite 53-66 |w (DE-627)315293152 |w (DE-600)2016909-7 |x 1573-1111 |7 nnns |
| 773 | 1 | 8 | |g volume:93 |g year:2018 |g number:1-2 |g day:21 |g month:08 |g pages:53-66 |
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10.1007/s10847-018-0835-8 doi (DE-627)SPR013727907 (SPR)s10847-018-0835-8-e DE-627 ger DE-627 rakwb eng 540 ASE 35.80 bkl 35.59 bkl Maeda, Yuki verfasserin aut Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. Cyclodextrins (dpeaa)DE-He213 GM1-gangliosidosis (dpeaa)DE-He213 GM1-ganglioside, cholesterol, lysosomes (dpeaa)DE-He213 Motoyama, Keiichi verfasserin aut Higashi, Taishi verfasserin aut Onodera, Risako verfasserin aut Takeo, Toru verfasserin aut Nakagata, Naomi verfasserin aut Kurauchi, Yuki verfasserin aut Katsuki, Hiroshi verfasserin aut Ishitsuka, Yoichi verfasserin aut Kondo, Yuki verfasserin aut Irie, Tetsumi verfasserin aut Era, Takumi verfasserin aut Arima, Hidetoshi verfasserin aut Enthalten in Journal of inclusion phenomena and macrocyclic chemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 93(2018), 1-2 vom: 21. Aug., Seite 53-66 (DE-627)315293152 (DE-600)2016909-7 1573-1111 nnns volume:93 year:2018 number:1-2 day:21 month:08 pages:53-66 https://dx.doi.org/10.1007/s10847-018-0835-8 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_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 35.80 ASE 35.59 ASE AR 93 2018 1-2 21 08 53-66 |
| spelling |
10.1007/s10847-018-0835-8 doi (DE-627)SPR013727907 (SPR)s10847-018-0835-8-e DE-627 ger DE-627 rakwb eng 540 ASE 35.80 bkl 35.59 bkl Maeda, Yuki verfasserin aut Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. Cyclodextrins (dpeaa)DE-He213 GM1-gangliosidosis (dpeaa)DE-He213 GM1-ganglioside, cholesterol, lysosomes (dpeaa)DE-He213 Motoyama, Keiichi verfasserin aut Higashi, Taishi verfasserin aut Onodera, Risako verfasserin aut Takeo, Toru verfasserin aut Nakagata, Naomi verfasserin aut Kurauchi, Yuki verfasserin aut Katsuki, Hiroshi verfasserin aut Ishitsuka, Yoichi verfasserin aut Kondo, Yuki verfasserin aut Irie, Tetsumi verfasserin aut Era, Takumi verfasserin aut Arima, Hidetoshi verfasserin aut Enthalten in Journal of inclusion phenomena and macrocyclic chemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 93(2018), 1-2 vom: 21. Aug., Seite 53-66 (DE-627)315293152 (DE-600)2016909-7 1573-1111 nnns volume:93 year:2018 number:1-2 day:21 month:08 pages:53-66 https://dx.doi.org/10.1007/s10847-018-0835-8 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_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 35.80 ASE 35.59 ASE AR 93 2018 1-2 21 08 53-66 |
| allfields_unstemmed |
10.1007/s10847-018-0835-8 doi (DE-627)SPR013727907 (SPR)s10847-018-0835-8-e DE-627 ger DE-627 rakwb eng 540 ASE 35.80 bkl 35.59 bkl Maeda, Yuki verfasserin aut Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. Cyclodextrins (dpeaa)DE-He213 GM1-gangliosidosis (dpeaa)DE-He213 GM1-ganglioside, cholesterol, lysosomes (dpeaa)DE-He213 Motoyama, Keiichi verfasserin aut Higashi, Taishi verfasserin aut Onodera, Risako verfasserin aut Takeo, Toru verfasserin aut Nakagata, Naomi verfasserin aut Kurauchi, Yuki verfasserin aut Katsuki, Hiroshi verfasserin aut Ishitsuka, Yoichi verfasserin aut Kondo, Yuki verfasserin aut Irie, Tetsumi verfasserin aut Era, Takumi verfasserin aut Arima, Hidetoshi verfasserin aut Enthalten in Journal of inclusion phenomena and macrocyclic chemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 93(2018), 1-2 vom: 21. Aug., Seite 53-66 (DE-627)315293152 (DE-600)2016909-7 1573-1111 nnns volume:93 year:2018 number:1-2 day:21 month:08 pages:53-66 https://dx.doi.org/10.1007/s10847-018-0835-8 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_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 35.80 ASE 35.59 ASE AR 93 2018 1-2 21 08 53-66 |
| allfieldsGer |
10.1007/s10847-018-0835-8 doi (DE-627)SPR013727907 (SPR)s10847-018-0835-8-e DE-627 ger DE-627 rakwb eng 540 ASE 35.80 bkl 35.59 bkl Maeda, Yuki verfasserin aut Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. Cyclodextrins (dpeaa)DE-He213 GM1-gangliosidosis (dpeaa)DE-He213 GM1-ganglioside, cholesterol, lysosomes (dpeaa)DE-He213 Motoyama, Keiichi verfasserin aut Higashi, Taishi verfasserin aut Onodera, Risako verfasserin aut Takeo, Toru verfasserin aut Nakagata, Naomi verfasserin aut Kurauchi, Yuki verfasserin aut Katsuki, Hiroshi verfasserin aut Ishitsuka, Yoichi verfasserin aut Kondo, Yuki verfasserin aut Irie, Tetsumi verfasserin aut Era, Takumi verfasserin aut Arima, Hidetoshi verfasserin aut Enthalten in Journal of inclusion phenomena and macrocyclic chemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 93(2018), 1-2 vom: 21. Aug., Seite 53-66 (DE-627)315293152 (DE-600)2016909-7 1573-1111 nnns volume:93 year:2018 number:1-2 day:21 month:08 pages:53-66 https://dx.doi.org/10.1007/s10847-018-0835-8 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_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 35.80 ASE 35.59 ASE AR 93 2018 1-2 21 08 53-66 |
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10.1007/s10847-018-0835-8 doi (DE-627)SPR013727907 (SPR)s10847-018-0835-8-e DE-627 ger DE-627 rakwb eng 540 ASE 35.80 bkl 35.59 bkl Maeda, Yuki verfasserin aut Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. Cyclodextrins (dpeaa)DE-He213 GM1-gangliosidosis (dpeaa)DE-He213 GM1-ganglioside, cholesterol, lysosomes (dpeaa)DE-He213 Motoyama, Keiichi verfasserin aut Higashi, Taishi verfasserin aut Onodera, Risako verfasserin aut Takeo, Toru verfasserin aut Nakagata, Naomi verfasserin aut Kurauchi, Yuki verfasserin aut Katsuki, Hiroshi verfasserin aut Ishitsuka, Yoichi verfasserin aut Kondo, Yuki verfasserin aut Irie, Tetsumi verfasserin aut Era, Takumi verfasserin aut Arima, Hidetoshi verfasserin aut Enthalten in Journal of inclusion phenomena and macrocyclic chemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983 93(2018), 1-2 vom: 21. Aug., Seite 53-66 (DE-627)315293152 (DE-600)2016909-7 1573-1111 nnns volume:93 year:2018 number:1-2 day:21 month:08 pages:53-66 https://dx.doi.org/10.1007/s10847-018-0835-8 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_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 35.80 ASE 35.59 ASE AR 93 2018 1-2 21 08 53-66 |
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Cyclodextrins GM1-gangliosidosis GM1-ganglioside, cholesterol, lysosomes |
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Maeda, Yuki @@aut@@ Motoyama, Keiichi @@aut@@ Higashi, Taishi @@aut@@ Onodera, Risako @@aut@@ Takeo, Toru @@aut@@ Nakagata, Naomi @@aut@@ Kurauchi, Yuki @@aut@@ Katsuki, Hiroshi @@aut@@ Ishitsuka, Yoichi @@aut@@ Kondo, Yuki @@aut@@ Irie, Tetsumi @@aut@@ Era, Takumi @@aut@@ Arima, Hidetoshi @@aut@@ |
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2018-08-21T00:00:00Z |
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| author |
Maeda, Yuki |
| spellingShingle |
Maeda, Yuki ddc 540 bkl 35.80 bkl 35.59 misc Cyclodextrins misc GM1-gangliosidosis misc GM1-ganglioside, cholesterol, lysosomes Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
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540 ASE 35.80 bkl 35.59 bkl Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice Cyclodextrins (dpeaa)DE-He213 GM1-gangliosidosis (dpeaa)DE-He213 GM1-ganglioside, cholesterol, lysosomes (dpeaa)DE-He213 |
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ddc 540 bkl 35.80 bkl 35.59 misc Cyclodextrins misc GM1-gangliosidosis misc GM1-ganglioside, cholesterol, lysosomes |
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ddc 540 bkl 35.80 bkl 35.59 misc Cyclodextrins misc GM1-gangliosidosis misc GM1-ganglioside, cholesterol, lysosomes |
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ddc 540 bkl 35.80 bkl 35.59 misc Cyclodextrins misc GM1-gangliosidosis misc GM1-ganglioside, cholesterol, lysosomes |
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Journal of inclusion phenomena and macrocyclic chemistry |
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Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
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Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
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Maeda, Yuki |
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Journal of inclusion phenomena and macrocyclic chemistry |
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Maeda, Yuki Motoyama, Keiichi Higashi, Taishi Onodera, Risako Takeo, Toru Nakagata, Naomi Kurauchi, Yuki Katsuki, Hiroshi Ishitsuka, Yoichi Kondo, Yuki Irie, Tetsumi Era, Takumi Arima, Hidetoshi |
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| title_sort |
lowering effect of dimethyl-α-cyclodextrin on gm1-ganglioside accumulation in gm1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
| title_auth |
Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
| abstract |
Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. |
| abstractGer |
Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. |
| abstract_unstemmed |
Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. Collectively, DM-α-CyD may have the potential as a therapeutic drug for GM1G. |
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Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice |
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Motoyama, Keiichi Higashi, Taishi Onodera, Risako Takeo, Toru Nakagata, Naomi Kurauchi, Yuki Katsuki, Hiroshi Ishitsuka, Yoichi Kondo, Yuki Irie, Tetsumi Era, Takumi Arima, Hidetoshi |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR013727907</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519194057.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201006s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s10847-018-0835-8</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR013727907</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s10847-018-0835-8-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">540</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">35.80</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">35.59</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Maeda, Yuki</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Lowering effect of dimethyl-α-cyclodextrin on GM1-ganglioside accumulation in GM1-gangliosidosis model cells and in brain of β-galactosidase-knockout mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract GM1-gangliosidosis (GM1G) is caused by a deficiency of β-galactosidase, resulting in the excessive accumulation of GM1-ganglioside (GM1) in lysosomes of cells, particularly in the nerve cells (neurons). There is no treatment available for patients with GM1G. Meanwhile, cyclodextrins (CyDs) are cyclic oligosaccharides, which are widely used in the pharmaceutical field. We previously reported that 2, 6-di-O-methyl-α-CyD (DM-α-CyD) extracted phospholipids from lipid rafts, which are abundant with sphingolipids including GM1. Therefore, in the present study, we investigated the effects of α-CyDs on GM1 levels in GM1G model cells and in brain of GM1G model mice. The interaction of DM-α-CyD with GM1 was stronger than that of 2-hydroxypropyl-α-CyD. Additionally, DM-α-CyD significantly reduced GM1 levels in GM1G model cells at 1 mM for 24 h. Furthermore, DM-α-CyD decreased GM1 levels in brain after an intraventricular administration to GM1G model mice without any significant side effects. These results strongly suggest that DM-α-CyD decreased the accumulation of GM1 in not only GM1G model cells but also GM1G model mice. 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