Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression

Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of...
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Autor*in:	Acquaviva, Fabio [verfasserIn] Castaldo, Imma Filla, Alessandro Giacchetti, Manuela Marmolino, Daniele Monticelli, Antonella Pinelli, Michele Saccà, Francesco Cocozza, Sergio

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2008

Schlagwörter:	Friedreich’s ataxia Frataxin Erythropoietin

Anmerkung:	© Springer Science+Business Media, LLC 2008

Übergeordnetes Werk:	Enthalten in: The Cerebellum - London : Dunitz, 2002, 7(2008), 3 vom: 26. Juni, Seite 360-365
Übergeordnetes Werk:	volume:7 ; year:2008 ; number:3 ; day:26 ; month:06 ; pages:360-365

Links:	Volltext

DOI / URN:	10.1007/s12311-008-0036-x

Katalog-ID:	SPR024898295

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520			\|a Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia.
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912			\|a GBV_ILN_281
912			\|a GBV_ILN_285
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912			\|a GBV_ILN_602
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912			\|a GBV_ILN_2039
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
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912			\|a GBV_ILN_2057
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912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2070
912			\|a GBV_ILN_2086
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912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2107
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author_variant	f a fa i c ic a f af m g mg d m dm a m am m p mp f s fs s c sc
matchkey_str	article:14734230:2008----::eobnnhmnrtrpitnnraefaaipoenxrsinih
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publishDate	2008
allfields	10.1007/s12311-008-0036-x doi (DE-627)SPR024898295 (SPR)s12311-008-0036-x-e DE-627 ger DE-627 rakwb eng Acquaviva, Fabio verfasserin aut Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2008 Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. Friedreich’s ataxia (dpeaa)DE-He213 Frataxin (dpeaa)DE-He213 Erythropoietin (dpeaa)DE-He213 Castaldo, Imma aut Filla, Alessandro aut Giacchetti, Manuela aut Marmolino, Daniele aut Monticelli, Antonella aut Pinelli, Michele aut Saccà, Francesco aut Cocozza, Sergio aut Enthalten in The Cerebellum London : Dunitz, 2002 7(2008), 3 vom: 26. Juni, Seite 360-365 (DE-627)342317237 (DE-600)2071266-2 1473-4230 nnns volume:7 year:2008 number:3 day:26 month:06 pages:360-365 https://dx.doi.org/10.1007/s12311-008-0036-x 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_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 7 2008 3 26 06 360-365
spelling	10.1007/s12311-008-0036-x doi (DE-627)SPR024898295 (SPR)s12311-008-0036-x-e DE-627 ger DE-627 rakwb eng Acquaviva, Fabio verfasserin aut Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2008 Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. Friedreich’s ataxia (dpeaa)DE-He213 Frataxin (dpeaa)DE-He213 Erythropoietin (dpeaa)DE-He213 Castaldo, Imma aut Filla, Alessandro aut Giacchetti, Manuela aut Marmolino, Daniele aut Monticelli, Antonella aut Pinelli, Michele aut Saccà, Francesco aut Cocozza, Sergio aut Enthalten in The Cerebellum London : Dunitz, 2002 7(2008), 3 vom: 26. Juni, Seite 360-365 (DE-627)342317237 (DE-600)2071266-2 1473-4230 nnns volume:7 year:2008 number:3 day:26 month:06 pages:360-365 https://dx.doi.org/10.1007/s12311-008-0036-x 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_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 7 2008 3 26 06 360-365
allfields_unstemmed	10.1007/s12311-008-0036-x doi (DE-627)SPR024898295 (SPR)s12311-008-0036-x-e DE-627 ger DE-627 rakwb eng Acquaviva, Fabio verfasserin aut Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2008 Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. Friedreich’s ataxia (dpeaa)DE-He213 Frataxin (dpeaa)DE-He213 Erythropoietin (dpeaa)DE-He213 Castaldo, Imma aut Filla, Alessandro aut Giacchetti, Manuela aut Marmolino, Daniele aut Monticelli, Antonella aut Pinelli, Michele aut Saccà, Francesco aut Cocozza, Sergio aut Enthalten in The Cerebellum London : Dunitz, 2002 7(2008), 3 vom: 26. Juni, Seite 360-365 (DE-627)342317237 (DE-600)2071266-2 1473-4230 nnns volume:7 year:2008 number:3 day:26 month:06 pages:360-365 https://dx.doi.org/10.1007/s12311-008-0036-x 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_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 7 2008 3 26 06 360-365
allfieldsGer	10.1007/s12311-008-0036-x doi (DE-627)SPR024898295 (SPR)s12311-008-0036-x-e DE-627 ger DE-627 rakwb eng Acquaviva, Fabio verfasserin aut Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2008 Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. Friedreich’s ataxia (dpeaa)DE-He213 Frataxin (dpeaa)DE-He213 Erythropoietin (dpeaa)DE-He213 Castaldo, Imma aut Filla, Alessandro aut Giacchetti, Manuela aut Marmolino, Daniele aut Monticelli, Antonella aut Pinelli, Michele aut Saccà, Francesco aut Cocozza, Sergio aut Enthalten in The Cerebellum London : Dunitz, 2002 7(2008), 3 vom: 26. Juni, Seite 360-365 (DE-627)342317237 (DE-600)2071266-2 1473-4230 nnns volume:7 year:2008 number:3 day:26 month:06 pages:360-365 https://dx.doi.org/10.1007/s12311-008-0036-x 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_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 7 2008 3 26 06 360-365
allfieldsSound	10.1007/s12311-008-0036-x doi (DE-627)SPR024898295 (SPR)s12311-008-0036-x-e DE-627 ger DE-627 rakwb eng Acquaviva, Fabio verfasserin aut Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2008 Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. Friedreich’s ataxia (dpeaa)DE-He213 Frataxin (dpeaa)DE-He213 Erythropoietin (dpeaa)DE-He213 Castaldo, Imma aut Filla, Alessandro aut Giacchetti, Manuela aut Marmolino, Daniele aut Monticelli, Antonella aut Pinelli, Michele aut Saccà, Francesco aut Cocozza, Sergio aut Enthalten in The Cerebellum London : Dunitz, 2002 7(2008), 3 vom: 26. Juni, Seite 360-365 (DE-627)342317237 (DE-600)2071266-2 1473-4230 nnns volume:7 year:2008 number:3 day:26 month:06 pages:360-365 https://dx.doi.org/10.1007/s12311-008-0036-x 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_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 7 2008 3 26 06 360-365
language	English
source	Enthalten in The Cerebellum 7(2008), 3 vom: 26. Juni, Seite 360-365 volume:7 year:2008 number:3 day:26 month:06 pages:360-365
sourceStr	Enthalten in The Cerebellum 7(2008), 3 vom: 26. Juni, Seite 360-365 volume:7 year:2008 number:3 day:26 month:06 pages:360-365
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Friedreich’s ataxia Frataxin Erythropoietin
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container_title	The Cerebellum
authorswithroles_txt_mv	Acquaviva, Fabio @@aut@@ Castaldo, Imma @@aut@@ Filla, Alessandro @@aut@@ Giacchetti, Manuela @@aut@@ Marmolino, Daniele @@aut@@ Monticelli, Antonella @@aut@@ Pinelli, Michele @@aut@@ Saccà, Francesco @@aut@@ Cocozza, Sergio @@aut@@
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author	Acquaviva, Fabio
spellingShingle	Acquaviva, Fabio misc Friedreich’s ataxia misc Frataxin misc Erythropoietin Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression
authorStr	Acquaviva, Fabio
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topic_title	Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression Friedreich’s ataxia (dpeaa)DE-He213 Frataxin (dpeaa)DE-He213 Erythropoietin (dpeaa)DE-He213
topic	misc Friedreich’s ataxia misc Frataxin misc Erythropoietin
topic_unstemmed	misc Friedreich’s ataxia misc Frataxin misc Erythropoietin
topic_browse	misc Friedreich’s ataxia misc Frataxin misc Erythropoietin
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title	Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression
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title_full	Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression
author_sort	Acquaviva, Fabio
journal	The Cerebellum
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author_browse	Acquaviva, Fabio Castaldo, Imma Filla, Alessandro Giacchetti, Manuela Marmolino, Daniele Monticelli, Antonella Pinelli, Michele Saccà, Francesco Cocozza, Sergio
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author-letter	Acquaviva, Fabio
doi_str_mv	10.1007/s12311-008-0036-x
title_sort	recombinant human erythropoietin increases frataxin protein expression without increasing mrna expression
title_auth	Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression
abstract	Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. © Springer Science+Business Media, LLC 2008
abstractGer	Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. © Springer Science+Business Media, LLC 2008
abstract_unstemmed	Abstract Friedreich’s ataxia is an autosomal recessive neurodegenerative disease that is due to the loss of function of the frataxin protein. The molecular basis of this disease is still a matter of debate and treatments have so far focused on managing symptoms. Drugs that can increase the amount of frataxin protein offer a possible therapy for the disease. One such drug is recombinant human erythropoietin (rhu-EPO). Here, we report the effects of rhu-EPO on frataxin mRNA and protein in primary fibroblast cell cultures derived from Friedreich’s ataxia patients. We observed a slight but significant increase in the amount of frataxin protein. Interestingly, we did not observe any increase in the messenger RNA expression at any of the times and doses tested, suggesting that the regulatory effects of rhu-EPO on the frataxin protein was at the post-translational level. These findings could help the evaluation of the treatment with erythropoietin as a potential therapeutic agent for Friedreich’s ataxia. © Springer Science+Business Media, LLC 2008
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container_issue	3
title_short	Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression
url	https://dx.doi.org/10.1007/s12311-008-0036-x
remote_bool	true
author2	Castaldo, Imma Filla, Alessandro Giacchetti, Manuela Marmolino, Daniele Monticelli, Antonella Pinelli, Michele Saccà, Francesco Cocozza, Sergio
author2Str	Castaldo, Imma Filla, Alessandro Giacchetti, Manuela Marmolino, Daniele Monticelli, Antonella Pinelli, Michele Saccà, Francesco Cocozza, Sergio
ppnlink	342317237
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doi_str	10.1007/s12311-008-0036-x
up_date	2024-07-04T02:46:18.926Z
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Recombinant Human Erythropoietin Increases Frataxin Protein Expression Without Increasing mRNA Expression

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