Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism
Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wista...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Teixeira, Rayane Brinck [verfasserIn] Barboza, Tatiane Evelyn [verfasserIn] de Araújo, Carla Cristina [verfasserIn] Siqueira, Rafaela [verfasserIn] de Castro, Alexandre Luz [verfasserIn] Bonetto, Jéssica Hellen Poletto [verfasserIn] de Lima-Seolin, Bruna Gazzi [verfasserIn] Carraro, Cristina Campos [verfasserIn] Belló-Klein, Adriane [verfasserIn] Singal, Pawan K [verfasserIn] da Rosa Araujo, Alex Sander [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 biosciences - Bangalore : Indian Acad. of Sciences, 1979, 43(2018), 5 vom: 06. Okt., Seite 887-895 |
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| Übergeordnetes Werk: |
volume:43 ; year:2018 ; number:5 ; day:06 ; month:10 ; pages:887-895 |
| Links: |
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| DOI / URN: |
10.1007/s12038-018-9816-8 |
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| Katalog-ID: |
SPR024022500 |
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| 245 | 1 | 0 | |a Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
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| 520 | |a Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. | ||
| 650 | 4 | |a Cardiac hypertrophy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a cell death |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a hyperthyroidism |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a inflammation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a PGC1-α |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Barboza, Tatiane Evelyn |e verfasserin |4 aut | |
| 700 | 1 | |a de Araújo, Carla Cristina |e verfasserin |4 aut | |
| 700 | 1 | |a Siqueira, Rafaela |e verfasserin |4 aut | |
| 700 | 1 | |a de Castro, Alexandre Luz |e verfasserin |4 aut | |
| 700 | 1 | |a Bonetto, Jéssica Hellen Poletto |e verfasserin |4 aut | |
| 700 | 1 | |a de Lima-Seolin, Bruna Gazzi |e verfasserin |4 aut | |
| 700 | 1 | |a Carraro, Cristina Campos |e verfasserin |4 aut | |
| 700 | 1 | |a Belló-Klein, Adriane |e verfasserin |4 aut | |
| 700 | 1 | |a Singal, Pawan K |e verfasserin |4 aut | |
| 700 | 1 | |a da Rosa Araujo, Alex Sander |e verfasserin |4 aut | |
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10.1007/s12038-018-9816-8 doi (DE-627)SPR024022500 (SPR)s12038-018-9816-8-e DE-627 ger DE-627 rakwb eng 570 ASE 42.00 bkl Teixeira, Rayane Brinck verfasserin aut Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. Cardiac hypertrophy (dpeaa)DE-He213 cell death (dpeaa)DE-He213 hyperthyroidism (dpeaa)DE-He213 inflammation (dpeaa)DE-He213 PGC1-α (dpeaa)DE-He213 Barboza, Tatiane Evelyn verfasserin aut de Araújo, Carla Cristina verfasserin aut Siqueira, Rafaela verfasserin aut de Castro, Alexandre Luz verfasserin aut Bonetto, Jéssica Hellen Poletto verfasserin aut de Lima-Seolin, Bruna Gazzi verfasserin aut Carraro, Cristina Campos verfasserin aut Belló-Klein, Adriane verfasserin aut Singal, Pawan K verfasserin aut da Rosa Araujo, Alex Sander verfasserin aut Enthalten in Journal of biosciences Bangalore : Indian Acad. of Sciences, 1979 43(2018), 5 vom: 06. Okt., Seite 887-895 (DE-627)342317474 (DE-600)2071290-X 0973-7138 nnns volume:43 year:2018 number:5 day:06 month:10 pages:887-895 https://dx.doi.org/10.1007/s12038-018-9816-8 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 42.00 ASE AR 43 2018 5 06 10 887-895 |
| spelling |
10.1007/s12038-018-9816-8 doi (DE-627)SPR024022500 (SPR)s12038-018-9816-8-e DE-627 ger DE-627 rakwb eng 570 ASE 42.00 bkl Teixeira, Rayane Brinck verfasserin aut Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. Cardiac hypertrophy (dpeaa)DE-He213 cell death (dpeaa)DE-He213 hyperthyroidism (dpeaa)DE-He213 inflammation (dpeaa)DE-He213 PGC1-α (dpeaa)DE-He213 Barboza, Tatiane Evelyn verfasserin aut de Araújo, Carla Cristina verfasserin aut Siqueira, Rafaela verfasserin aut de Castro, Alexandre Luz verfasserin aut Bonetto, Jéssica Hellen Poletto verfasserin aut de Lima-Seolin, Bruna Gazzi verfasserin aut Carraro, Cristina Campos verfasserin aut Belló-Klein, Adriane verfasserin aut Singal, Pawan K verfasserin aut da Rosa Araujo, Alex Sander verfasserin aut Enthalten in Journal of biosciences Bangalore : Indian Acad. of Sciences, 1979 43(2018), 5 vom: 06. Okt., Seite 887-895 (DE-627)342317474 (DE-600)2071290-X 0973-7138 nnns volume:43 year:2018 number:5 day:06 month:10 pages:887-895 https://dx.doi.org/10.1007/s12038-018-9816-8 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 42.00 ASE AR 43 2018 5 06 10 887-895 |
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10.1007/s12038-018-9816-8 doi (DE-627)SPR024022500 (SPR)s12038-018-9816-8-e DE-627 ger DE-627 rakwb eng 570 ASE 42.00 bkl Teixeira, Rayane Brinck verfasserin aut Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. Cardiac hypertrophy (dpeaa)DE-He213 cell death (dpeaa)DE-He213 hyperthyroidism (dpeaa)DE-He213 inflammation (dpeaa)DE-He213 PGC1-α (dpeaa)DE-He213 Barboza, Tatiane Evelyn verfasserin aut de Araújo, Carla Cristina verfasserin aut Siqueira, Rafaela verfasserin aut de Castro, Alexandre Luz verfasserin aut Bonetto, Jéssica Hellen Poletto verfasserin aut de Lima-Seolin, Bruna Gazzi verfasserin aut Carraro, Cristina Campos verfasserin aut Belló-Klein, Adriane verfasserin aut Singal, Pawan K verfasserin aut da Rosa Araujo, Alex Sander verfasserin aut Enthalten in Journal of biosciences Bangalore : Indian Acad. of Sciences, 1979 43(2018), 5 vom: 06. Okt., Seite 887-895 (DE-627)342317474 (DE-600)2071290-X 0973-7138 nnns volume:43 year:2018 number:5 day:06 month:10 pages:887-895 https://dx.doi.org/10.1007/s12038-018-9816-8 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 42.00 ASE AR 43 2018 5 06 10 887-895 |
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10.1007/s12038-018-9816-8 doi (DE-627)SPR024022500 (SPR)s12038-018-9816-8-e DE-627 ger DE-627 rakwb eng 570 ASE 42.00 bkl Teixeira, Rayane Brinck verfasserin aut Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. Cardiac hypertrophy (dpeaa)DE-He213 cell death (dpeaa)DE-He213 hyperthyroidism (dpeaa)DE-He213 inflammation (dpeaa)DE-He213 PGC1-α (dpeaa)DE-He213 Barboza, Tatiane Evelyn verfasserin aut de Araújo, Carla Cristina verfasserin aut Siqueira, Rafaela verfasserin aut de Castro, Alexandre Luz verfasserin aut Bonetto, Jéssica Hellen Poletto verfasserin aut de Lima-Seolin, Bruna Gazzi verfasserin aut Carraro, Cristina Campos verfasserin aut Belló-Klein, Adriane verfasserin aut Singal, Pawan K verfasserin aut da Rosa Araujo, Alex Sander verfasserin aut Enthalten in Journal of biosciences Bangalore : Indian Acad. of Sciences, 1979 43(2018), 5 vom: 06. Okt., Seite 887-895 (DE-627)342317474 (DE-600)2071290-X 0973-7138 nnns volume:43 year:2018 number:5 day:06 month:10 pages:887-895 https://dx.doi.org/10.1007/s12038-018-9816-8 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 42.00 ASE AR 43 2018 5 06 10 887-895 |
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10.1007/s12038-018-9816-8 doi (DE-627)SPR024022500 (SPR)s12038-018-9816-8-e DE-627 ger DE-627 rakwb eng 570 ASE 42.00 bkl Teixeira, Rayane Brinck verfasserin aut Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. Cardiac hypertrophy (dpeaa)DE-He213 cell death (dpeaa)DE-He213 hyperthyroidism (dpeaa)DE-He213 inflammation (dpeaa)DE-He213 PGC1-α (dpeaa)DE-He213 Barboza, Tatiane Evelyn verfasserin aut de Araújo, Carla Cristina verfasserin aut Siqueira, Rafaela verfasserin aut de Castro, Alexandre Luz verfasserin aut Bonetto, Jéssica Hellen Poletto verfasserin aut de Lima-Seolin, Bruna Gazzi verfasserin aut Carraro, Cristina Campos verfasserin aut Belló-Klein, Adriane verfasserin aut Singal, Pawan K verfasserin aut da Rosa Araujo, Alex Sander verfasserin aut Enthalten in Journal of biosciences Bangalore : Indian Acad. of Sciences, 1979 43(2018), 5 vom: 06. Okt., Seite 887-895 (DE-627)342317474 (DE-600)2071290-X 0973-7138 nnns volume:43 year:2018 number:5 day:06 month:10 pages:887-895 https://dx.doi.org/10.1007/s12038-018-9816-8 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 42.00 ASE AR 43 2018 5 06 10 887-895 |
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Enthalten in Journal of biosciences 43(2018), 5 vom: 06. Okt., Seite 887-895 volume:43 year:2018 number:5 day:06 month:10 pages:887-895 |
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Enthalten in Journal of biosciences 43(2018), 5 vom: 06. Okt., Seite 887-895 volume:43 year:2018 number:5 day:06 month:10 pages:887-895 |
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Cardiac hypertrophy cell death hyperthyroidism inflammation PGC1-α |
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Teixeira, Rayane Brinck @@aut@@ Barboza, Tatiane Evelyn @@aut@@ de Araújo, Carla Cristina @@aut@@ Siqueira, Rafaela @@aut@@ de Castro, Alexandre Luz @@aut@@ Bonetto, Jéssica Hellen Poletto @@aut@@ de Lima-Seolin, Bruna Gazzi @@aut@@ Carraro, Cristina Campos @@aut@@ Belló-Klein, Adriane @@aut@@ Singal, Pawan K @@aut@@ da Rosa Araujo, Alex Sander @@aut@@ |
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2018-10-06T00:00:00Z |
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This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. 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Teixeira, Rayane Brinck |
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Teixeira, Rayane Brinck ddc 570 bkl 42.00 misc Cardiac hypertrophy misc cell death misc hyperthyroidism misc inflammation misc PGC1-α Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
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Teixeira, Rayane Brinck |
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570 ASE 42.00 bkl Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism Cardiac hypertrophy (dpeaa)DE-He213 cell death (dpeaa)DE-He213 hyperthyroidism (dpeaa)DE-He213 inflammation (dpeaa)DE-He213 PGC1-α (dpeaa)DE-He213 |
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ddc 570 bkl 42.00 misc Cardiac hypertrophy misc cell death misc hyperthyroidism misc inflammation misc PGC1-α |
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ddc 570 bkl 42.00 misc Cardiac hypertrophy misc cell death misc hyperthyroidism misc inflammation misc PGC1-α |
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ddc 570 bkl 42.00 misc Cardiac hypertrophy misc cell death misc hyperthyroidism misc inflammation misc PGC1-α |
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Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
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| title_full |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
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Teixeira, Rayane Brinck |
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Journal of biosciences |
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Journal of biosciences |
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eng |
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Teixeira, Rayane Brinck Barboza, Tatiane Evelyn de Araújo, Carla Cristina Siqueira, Rafaela de Castro, Alexandre Luz Bonetto, Jéssica Hellen Poletto de Lima-Seolin, Bruna Gazzi Carraro, Cristina Campos Belló-Klein, Adriane Singal, Pawan K da Rosa Araujo, Alex Sander |
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Teixeira, Rayane Brinck |
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10.1007/s12038-018-9816-8 |
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570 |
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verfasserin |
| title_sort |
decreased pgc1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
| title_auth |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
| abstract |
Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. |
| abstractGer |
Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. |
| abstract_unstemmed |
Abstract Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy. |
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Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
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https://dx.doi.org/10.1007/s12038-018-9816-8 |
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Barboza, Tatiane Evelyn de Araújo, Carla Cristina Siqueira, Rafaela de Castro, Alexandre Luz Bonetto, Jéssica Hellen Poletto de Lima-Seolin, Bruna Gazzi Carraro, Cristina Campos Belló-Klein, Adriane Singal, Pawan K da Rosa Araujo, Alex Sander |
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Barboza, Tatiane Evelyn de Araújo, Carla Cristina Siqueira, Rafaela de Castro, Alexandre Luz Bonetto, Jéssica Hellen Poletto de Lima-Seolin, Bruna Gazzi Carraro, Cristina Campos Belló-Klein, Adriane Singal, Pawan K da Rosa Araujo, Alex Sander |
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| score |
7.3988447 |