Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin
Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhou, Jinfu [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Anmerkung: |
© The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Molecular biology reports - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973, 50(2023), 8 vom: 28. Juni, Seite 6703-6715 |
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| Übergeordnetes Werk: |
volume:50 ; year:2023 ; number:8 ; day:28 ; month:06 ; pages:6703-6715 |
| Links: |
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| DOI / URN: |
10.1007/s11033-023-08576-1 |
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| Katalog-ID: |
SPR052551040 |
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| 100 | 1 | |a Zhou, Jinfu |e verfasserin |0 (orcid)0000-0002-2078-8646 |4 aut | |
| 245 | 1 | 0 | |a Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin |
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| 520 | |a Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. | ||
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| 650 | 4 | |a Methylated RNA immunoprecipitation sequencing |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Li, Huangyuan |4 aut | |
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10.1007/s11033-023-08576-1 doi (DE-627)SPR052551040 (SPR)s11033-023-08576-1-e DE-627 ger DE-627 rakwb eng Zhou, Jinfu verfasserin (orcid)0000-0002-2078-8646 aut Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. -methyladenosine (dpeaa)DE-He213 Methylated RNA immunoprecipitation sequencing (dpeaa)DE-He213 Methylation (dpeaa)DE-He213 mRNA profile (dpeaa)DE-He213 Neurotoxicity (dpeaa)DE-He213 Unconjugated bilirubin (dpeaa)DE-He213 Liao, Sining aut Zhang, Chenran aut Luo, Jinying aut Li, Guilin aut Li, Huangyuan aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 50(2023), 8 vom: 28. Juni, Seite 6703-6715 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:50 year:2023 number:8 day:28 month:06 pages:6703-6715 https://dx.doi.org/10.1007/s11033-023-08576-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 50 2023 8 28 06 6703-6715 |
| spelling |
10.1007/s11033-023-08576-1 doi (DE-627)SPR052551040 (SPR)s11033-023-08576-1-e DE-627 ger DE-627 rakwb eng Zhou, Jinfu verfasserin (orcid)0000-0002-2078-8646 aut Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. -methyladenosine (dpeaa)DE-He213 Methylated RNA immunoprecipitation sequencing (dpeaa)DE-He213 Methylation (dpeaa)DE-He213 mRNA profile (dpeaa)DE-He213 Neurotoxicity (dpeaa)DE-He213 Unconjugated bilirubin (dpeaa)DE-He213 Liao, Sining aut Zhang, Chenran aut Luo, Jinying aut Li, Guilin aut Li, Huangyuan aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 50(2023), 8 vom: 28. Juni, Seite 6703-6715 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:50 year:2023 number:8 day:28 month:06 pages:6703-6715 https://dx.doi.org/10.1007/s11033-023-08576-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 50 2023 8 28 06 6703-6715 |
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10.1007/s11033-023-08576-1 doi (DE-627)SPR052551040 (SPR)s11033-023-08576-1-e DE-627 ger DE-627 rakwb eng Zhou, Jinfu verfasserin (orcid)0000-0002-2078-8646 aut Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. -methyladenosine (dpeaa)DE-He213 Methylated RNA immunoprecipitation sequencing (dpeaa)DE-He213 Methylation (dpeaa)DE-He213 mRNA profile (dpeaa)DE-He213 Neurotoxicity (dpeaa)DE-He213 Unconjugated bilirubin (dpeaa)DE-He213 Liao, Sining aut Zhang, Chenran aut Luo, Jinying aut Li, Guilin aut Li, Huangyuan aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 50(2023), 8 vom: 28. Juni, Seite 6703-6715 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:50 year:2023 number:8 day:28 month:06 pages:6703-6715 https://dx.doi.org/10.1007/s11033-023-08576-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 50 2023 8 28 06 6703-6715 |
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10.1007/s11033-023-08576-1 doi (DE-627)SPR052551040 (SPR)s11033-023-08576-1-e DE-627 ger DE-627 rakwb eng Zhou, Jinfu verfasserin (orcid)0000-0002-2078-8646 aut Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. -methyladenosine (dpeaa)DE-He213 Methylated RNA immunoprecipitation sequencing (dpeaa)DE-He213 Methylation (dpeaa)DE-He213 mRNA profile (dpeaa)DE-He213 Neurotoxicity (dpeaa)DE-He213 Unconjugated bilirubin (dpeaa)DE-He213 Liao, Sining aut Zhang, Chenran aut Luo, Jinying aut Li, Guilin aut Li, Huangyuan aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 50(2023), 8 vom: 28. Juni, Seite 6703-6715 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:50 year:2023 number:8 day:28 month:06 pages:6703-6715 https://dx.doi.org/10.1007/s11033-023-08576-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 50 2023 8 28 06 6703-6715 |
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10.1007/s11033-023-08576-1 doi (DE-627)SPR052551040 (SPR)s11033-023-08576-1-e DE-627 ger DE-627 rakwb eng Zhou, Jinfu verfasserin (orcid)0000-0002-2078-8646 aut Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. -methyladenosine (dpeaa)DE-He213 Methylated RNA immunoprecipitation sequencing (dpeaa)DE-He213 Methylation (dpeaa)DE-He213 mRNA profile (dpeaa)DE-He213 Neurotoxicity (dpeaa)DE-He213 Unconjugated bilirubin (dpeaa)DE-He213 Liao, Sining aut Zhang, Chenran aut Luo, Jinying aut Li, Guilin aut Li, Huangyuan aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 50(2023), 8 vom: 28. Juni, Seite 6703-6715 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:50 year:2023 number:8 day:28 month:06 pages:6703-6715 https://dx.doi.org/10.1007/s11033-023-08576-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 50 2023 8 28 06 6703-6715 |
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Enthalten in Molecular biology reports 50(2023), 8 vom: 28. Juni, Seite 6703-6715 volume:50 year:2023 number:8 day:28 month:06 pages:6703-6715 |
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-methyladenosine Methylated RNA immunoprecipitation sequencing Methylation mRNA profile Neurotoxicity Unconjugated bilirubin |
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Zhou, Jinfu @@aut@@ Liao, Sining @@aut@@ Zhang, Chenran @@aut@@ Luo, Jinying @@aut@@ Li, Guilin @@aut@@ Li, Huangyuan @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR052551040</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230728064721.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230728s2023 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s11033-023-08576-1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR052551040</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s11033-023-08576-1-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Zhou, Jinfu</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-2078-8646</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">-methyladenosine</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Methylated RNA immunoprecipitation sequencing</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Methylation</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">mRNA profile</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Neurotoxicity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Unconjugated bilirubin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liao, Sining</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Chenran</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Luo, Jinying</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Guilin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Huangyuan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Molecular biology reports</subfield><subfield code="d">Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973</subfield><subfield code="g">50(2023), 8 vom: 28. 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Zhou, Jinfu |
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Zhou, Jinfu misc -methyladenosine misc Methylated RNA immunoprecipitation sequencing misc Methylation misc mRNA profile misc Neurotoxicity misc Unconjugated bilirubin Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin |
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Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin -methyladenosine (dpeaa)DE-He213 Methylated RNA immunoprecipitation sequencing (dpeaa)DE-He213 Methylation (dpeaa)DE-He213 mRNA profile (dpeaa)DE-He213 Neurotoxicity (dpeaa)DE-He213 Unconjugated bilirubin (dpeaa)DE-He213 |
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misc -methyladenosine misc Methylated RNA immunoprecipitation sequencing misc Methylation misc mRNA profile misc Neurotoxicity misc Unconjugated bilirubin |
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misc -methyladenosine misc Methylated RNA immunoprecipitation sequencing misc Methylation misc mRNA profile misc Neurotoxicity misc Unconjugated bilirubin |
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misc -methyladenosine misc Methylated RNA immunoprecipitation sequencing misc Methylation misc mRNA profile misc Neurotoxicity misc Unconjugated bilirubin |
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Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin |
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Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin |
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Molecular biology reports |
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Zhou, Jinfu Liao, Sining Zhang, Chenran Luo, Jinying Li, Guilin Li, Huangyuan |
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expression profiling of n6-methyladenosine-modified mrna in pc12 cells in response to unconjugated bilirubin |
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Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin |
| abstract |
Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Background Abnormal methylation of N6-methyladenosine ($ m^{6} $A) is reportedly associated with central nervous system disorders. However, the role of $ m^{6} $A mRNA methylation in unconjugated bilirubin (UCB) neurotoxicity requires further research. Methods Rat pheochromocytoma PC12 cells treated with UCB were used as in vitro models. After the PC12 cells were treated with UCB (0, 12, 18, and 24 µM) for 24 h, the total RNA $ m^{6} $A levels were measured using an $ m^{6} $A RNA methylation quantification kit. The expression of m6A demethylases and methyltransferases was detected through western blotting. We determined the $ m^{6} $A mRNA methylation profile in PC12 cells exposed to UCB (0 and 18 µM) for 24 h using methylated RNA immunoprecipitation sequencing (MeRIP-seq). Results Compared with the control group, UCB (18 and 24 µM) treatment decreased the expression of the $ m^{6} $A demethylase ALKBH5 and increased the expression of the methyltransferases METTL3 and METTL14, which resulted in an increase in the total $ m^{6} $A levels in PC12 cells. Furthermore, 1533 $ m^{6} $A peaks were significantly elevated and 1331 peaks were reduced in the UCB (18 µM)-treated groups compared with those in the control group. Genes with differential $ m^{6} $A peaks were mainly enriched in protein processing in the endoplasmic reticulum, ubiquitin-mediated proteolysis, cell cycle, and endocytosis. Through combined analysis of the MeRIP-seq and RNA sequencing data, 129 genes with differentially methylated $ m^{6} $A peaks and differentially expressed mRNA levels were identified. Conclusion Our study suggests that the modulation of $ m^{6} $A methylation modifications plays a significant role in UCB neurotoxicity. © The Author(s) 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin |
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https://dx.doi.org/10.1007/s11033-023-08576-1 |
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Liao, Sining Zhang, Chenran Luo, Jinying Li, Guilin Li, Huangyuan |
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Liao, Sining Zhang, Chenran Luo, Jinying Li, Guilin Li, Huangyuan |
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2024-07-04T03:11:47.524Z |
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| score |
7.3980913 |