Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106
Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progres...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Heejin Lee [verfasserIn] Hye‐Ji Kim [verfasserIn] Dong‐Kyu Choi [verfasserIn] Eu n.‐A. Ko [verfasserIn] Jae‐Hyeog Choi [verfasserIn] Yohan Seo [verfasserIn] Sion Lee [verfasserIn] Soong‐Hyun Kim [verfasserIn] Sejin Jung [verfasserIn] Minwoo Kim [verfasserIn] Dongwan Kang [verfasserIn] Chun‐Young Im [verfasserIn] Gi‐Hun Bae [verfasserIn] Sung‐Cherl Jung [verfasserIn] Oh‐Bin Kwon [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Pharmacology Research & Perspectives - Wiley, 2016, 11(2023), 5, Seite n/a-n/a |
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| Übergeordnetes Werk: |
volume:11 ; year:2023 ; number:5 ; pages:n/a-n/a |
| Links: |
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| DOI / URN: |
10.1002/prp2.1135 |
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| Katalog-ID: |
DOAJ090927567 |
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| 245 | 1 | 0 | |a Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 |
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| 520 | |a Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. | ||
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10.1002/prp2.1135 doi (DE-627)DOAJ090927567 (DE-599)DOAJa831498fedc040b8a74e3e58dc2baca1 DE-627 ger DE-627 rakwb eng RM1-950 Heejin Lee verfasserin aut Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. ADHD dopamine HDACI VMAT2 Therapeutics. Pharmacology Hye‐Ji Kim verfasserin aut Dong‐Kyu Choi verfasserin aut Eu n.‐A. Ko verfasserin aut Jae‐Hyeog Choi verfasserin aut Yohan Seo verfasserin aut Sion Lee verfasserin aut Soong‐Hyun Kim verfasserin aut Sejin Jung verfasserin aut Minwoo Kim verfasserin aut Dongwan Kang verfasserin aut Chun‐Young Im verfasserin aut Gi‐Hun Bae verfasserin aut Sung‐Cherl Jung verfasserin aut Oh‐Bin Kwon verfasserin aut In Pharmacology Research & Perspectives Wiley, 2016 11(2023), 5, Seite n/a-n/a (DE-627)771394683 (DE-600)2740389-0 20521707 nnns volume:11 year:2023 number:5 pages:n/a-n/a https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/article/a831498fedc040b8a74e3e58dc2baca1 kostenfrei https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/toc/2052-1707 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 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_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4367 GBV_ILN_4700 AR 11 2023 5 n/a-n/a |
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10.1002/prp2.1135 doi (DE-627)DOAJ090927567 (DE-599)DOAJa831498fedc040b8a74e3e58dc2baca1 DE-627 ger DE-627 rakwb eng RM1-950 Heejin Lee verfasserin aut Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. ADHD dopamine HDACI VMAT2 Therapeutics. Pharmacology Hye‐Ji Kim verfasserin aut Dong‐Kyu Choi verfasserin aut Eu n.‐A. Ko verfasserin aut Jae‐Hyeog Choi verfasserin aut Yohan Seo verfasserin aut Sion Lee verfasserin aut Soong‐Hyun Kim verfasserin aut Sejin Jung verfasserin aut Minwoo Kim verfasserin aut Dongwan Kang verfasserin aut Chun‐Young Im verfasserin aut Gi‐Hun Bae verfasserin aut Sung‐Cherl Jung verfasserin aut Oh‐Bin Kwon verfasserin aut In Pharmacology Research & Perspectives Wiley, 2016 11(2023), 5, Seite n/a-n/a (DE-627)771394683 (DE-600)2740389-0 20521707 nnns volume:11 year:2023 number:5 pages:n/a-n/a https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/article/a831498fedc040b8a74e3e58dc2baca1 kostenfrei https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/toc/2052-1707 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 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_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4367 GBV_ILN_4700 AR 11 2023 5 n/a-n/a |
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10.1002/prp2.1135 doi (DE-627)DOAJ090927567 (DE-599)DOAJa831498fedc040b8a74e3e58dc2baca1 DE-627 ger DE-627 rakwb eng RM1-950 Heejin Lee verfasserin aut Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. ADHD dopamine HDACI VMAT2 Therapeutics. Pharmacology Hye‐Ji Kim verfasserin aut Dong‐Kyu Choi verfasserin aut Eu n.‐A. Ko verfasserin aut Jae‐Hyeog Choi verfasserin aut Yohan Seo verfasserin aut Sion Lee verfasserin aut Soong‐Hyun Kim verfasserin aut Sejin Jung verfasserin aut Minwoo Kim verfasserin aut Dongwan Kang verfasserin aut Chun‐Young Im verfasserin aut Gi‐Hun Bae verfasserin aut Sung‐Cherl Jung verfasserin aut Oh‐Bin Kwon verfasserin aut In Pharmacology Research & Perspectives Wiley, 2016 11(2023), 5, Seite n/a-n/a (DE-627)771394683 (DE-600)2740389-0 20521707 nnns volume:11 year:2023 number:5 pages:n/a-n/a https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/article/a831498fedc040b8a74e3e58dc2baca1 kostenfrei https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/toc/2052-1707 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 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_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4367 GBV_ILN_4700 AR 11 2023 5 n/a-n/a |
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10.1002/prp2.1135 doi (DE-627)DOAJ090927567 (DE-599)DOAJa831498fedc040b8a74e3e58dc2baca1 DE-627 ger DE-627 rakwb eng RM1-950 Heejin Lee verfasserin aut Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. ADHD dopamine HDACI VMAT2 Therapeutics. Pharmacology Hye‐Ji Kim verfasserin aut Dong‐Kyu Choi verfasserin aut Eu n.‐A. Ko verfasserin aut Jae‐Hyeog Choi verfasserin aut Yohan Seo verfasserin aut Sion Lee verfasserin aut Soong‐Hyun Kim verfasserin aut Sejin Jung verfasserin aut Minwoo Kim verfasserin aut Dongwan Kang verfasserin aut Chun‐Young Im verfasserin aut Gi‐Hun Bae verfasserin aut Sung‐Cherl Jung verfasserin aut Oh‐Bin Kwon verfasserin aut In Pharmacology Research & Perspectives Wiley, 2016 11(2023), 5, Seite n/a-n/a (DE-627)771394683 (DE-600)2740389-0 20521707 nnns volume:11 year:2023 number:5 pages:n/a-n/a https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/article/a831498fedc040b8a74e3e58dc2baca1 kostenfrei https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/toc/2052-1707 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 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_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4367 GBV_ILN_4700 AR 11 2023 5 n/a-n/a |
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10.1002/prp2.1135 doi (DE-627)DOAJ090927567 (DE-599)DOAJa831498fedc040b8a74e3e58dc2baca1 DE-627 ger DE-627 rakwb eng RM1-950 Heejin Lee verfasserin aut Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. ADHD dopamine HDACI VMAT2 Therapeutics. Pharmacology Hye‐Ji Kim verfasserin aut Dong‐Kyu Choi verfasserin aut Eu n.‐A. Ko verfasserin aut Jae‐Hyeog Choi verfasserin aut Yohan Seo verfasserin aut Sion Lee verfasserin aut Soong‐Hyun Kim verfasserin aut Sejin Jung verfasserin aut Minwoo Kim verfasserin aut Dongwan Kang verfasserin aut Chun‐Young Im verfasserin aut Gi‐Hun Bae verfasserin aut Sung‐Cherl Jung verfasserin aut Oh‐Bin Kwon verfasserin aut In Pharmacology Research & Perspectives Wiley, 2016 11(2023), 5, Seite n/a-n/a (DE-627)771394683 (DE-600)2740389-0 20521707 nnns volume:11 year:2023 number:5 pages:n/a-n/a https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/article/a831498fedc040b8a74e3e58dc2baca1 kostenfrei https://doi.org/10.1002/prp2.1135 kostenfrei https://doaj.org/toc/2052-1707 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 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_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4367 GBV_ILN_4700 AR 11 2023 5 n/a-n/a |
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Heejin Lee @@aut@@ Hye‐Ji Kim @@aut@@ Dong‐Kyu Choi @@aut@@ Eu n.‐A. Ko @@aut@@ Jae‐Hyeog Choi @@aut@@ Yohan Seo @@aut@@ Sion Lee @@aut@@ Soong‐Hyun Kim @@aut@@ Sejin Jung @@aut@@ Minwoo Kim @@aut@@ Dongwan Kang @@aut@@ Chun‐Young Im @@aut@@ Gi‐Hun Bae @@aut@@ Sung‐Cherl Jung @@aut@@ Oh‐Bin Kwon @@aut@@ |
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The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. 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RM1-950 Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 ADHD dopamine HDACI VMAT2 |
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Heejin Lee Hye‐Ji Kim Dong‐Kyu Choi Eu n.‐A. Ko Jae‐Hyeog Choi Yohan Seo Sion Lee Soong‐Hyun Kim Sejin Jung Minwoo Kim Dongwan Kang Chun‐Young Im Gi‐Hun Bae Sung‐Cherl Jung Oh‐Bin Kwon |
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dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by vmat2 expression through the class i hdac inhibitor tc‐h 106 |
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Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 |
| abstract |
Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. |
| abstractGer |
Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. |
| abstract_unstemmed |
Abstract The importance of vesicular monoamine transporter 2 (VMAT2) in dopamine regulation, which is considered crucial for neuropsychiatric disorders, is currently being studied. Moreover, the development of disease treatments using histone deacetylase (HDAC) inhibitors (HDACi) is actively progressing in various fields. Recently, research on the possibility of regulating neuropsychiatric disorders has been conducted. In this study, we evaluated whether VMAT2 expression increased by an HDACi can fine‐tune neuropsychotic behavior, such as attention deficit hyperactivity disorder (ADHD) and protect against the cell toxicity through oxidized dopamine. First, approximately 300 candidate HDACi compounds were added to the SH‐SY5Y dopaminergic cell line to identify the possible changes in the VMAT2 expression levels, which were measured using quantitative polymerase chain reaction. The results demonstrated, that treatment with pimelic diphenylamide 106 (TC‐H 106), a class I HDACi, increased VMAT2 expression in both the SH‐SY5Y cells and mouse brain. The increased VMAT2 expression induced by TC‐H 106 alleviated the cytotoxicity attributed to 6‐hydroxydopamine (6‐OHDA) or 1‐methyl‐4‐phenylpyridinium (MPP+) and free dopamine treatment. Moreover, dopamine concentrations, both intracellularly and in the synaptosomes, were significantly elevated by increased VMAT2 expression. These results suggest that dopamine concentration regulation by VMAT2 expression induced by TC‐H 106 could alter several related behavioral aspects that was confirmed by attenuation of hyperactivity and impulsivity, which were major characteristics of animal model showing ADHD‐like behaviors. These results indicate that HDACi‐increased VMAT2 expression offers sufficient protections against dopaminergic cell death induced by oxidative stress. Thus, the epigenetic approach could be considered as therapeutic candidate for neuropsychiatric disease regulation. |
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Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106 |
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https://doi.org/10.1002/prp2.1135 https://doaj.org/article/a831498fedc040b8a74e3e58dc2baca1 https://doaj.org/toc/2052-1707 |
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Hye‐Ji Kim Dong‐Kyu Choi Eu n.‐A. Ko Jae‐Hyeog Choi Yohan Seo Sion Lee Soong‐Hyun Kim Sejin Jung Minwoo Kim Dongwan Kang Chun‐Young Im Gi‐Hun Bae Sung‐Cherl Jung Oh‐Bin Kwon |
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Hye‐Ji Kim Dong‐Kyu Choi Eu n.‐A. Ko Jae‐Hyeog Choi Yohan Seo Sion Lee Soong‐Hyun Kim Sejin Jung Minwoo Kim Dongwan Kang Chun‐Young Im Gi‐Hun Bae Sung‐Cherl Jung Oh‐Bin Kwon |
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RM - Therapeutics and Pharmacology |
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10.1002/prp2.1135 |
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