Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken
Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Feng, Yue [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Anmerkung: |
© Cell Stress Society International 2019 |
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| Übergeordnetes Werk: |
Enthalten in: Cell stress & chaperones - Dordrecht : Springer, 1996, 25(2019), 1 vom: 19. Nov., Seite 47-56 |
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| Übergeordnetes Werk: |
volume:25 ; year:2019 ; number:1 ; day:19 ; month:11 ; pages:47-56 |
| Links: |
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| DOI / URN: |
10.1007/s12192-019-01034-7 |
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| Katalog-ID: |
SPR025171623 |
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| 100 | 1 | |a Feng, Yue |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken |
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| 520 | |a Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. | ||
| 650 | 4 | |a Chicken liver |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Inflammation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Fibrosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Heat shock proteins |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a N6-methyladenosine |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Hu, Yun |4 aut | |
| 700 | 1 | |a Hou, Zhen |4 aut | |
| 700 | 1 | |a Sun, Qinwei |4 aut | |
| 700 | 1 | |a Jia, Yimin |4 aut | |
| 700 | 1 | |a Zhao, Ruqian |4 aut | |
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10.1007/s12192-019-01034-7 doi (DE-627)SPR025171623 (SPR)s12192-019-01034-7-e DE-627 ger DE-627 rakwb eng Feng, Yue verfasserin aut Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cell Stress Society International 2019 Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. Chicken liver (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Heat shock proteins (dpeaa)DE-He213 N6-methyladenosine (dpeaa)DE-He213 Hu, Yun aut Hou, Zhen aut Sun, Qinwei aut Jia, Yimin aut Zhao, Ruqian aut Enthalten in Cell stress & chaperones Dordrecht : Springer, 1996 25(2019), 1 vom: 19. Nov., Seite 47-56 (DE-627)320421309 (DE-600)2002594-4 1466-1268 nnns volume:25 year:2019 number:1 day:19 month:11 pages:47-56 https://dx.doi.org/10.1007/s12192-019-01034-7 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_165 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_374 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_2018 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_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2019 1 19 11 47-56 |
| spelling |
10.1007/s12192-019-01034-7 doi (DE-627)SPR025171623 (SPR)s12192-019-01034-7-e DE-627 ger DE-627 rakwb eng Feng, Yue verfasserin aut Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cell Stress Society International 2019 Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. Chicken liver (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Heat shock proteins (dpeaa)DE-He213 N6-methyladenosine (dpeaa)DE-He213 Hu, Yun aut Hou, Zhen aut Sun, Qinwei aut Jia, Yimin aut Zhao, Ruqian aut Enthalten in Cell stress & chaperones Dordrecht : Springer, 1996 25(2019), 1 vom: 19. Nov., Seite 47-56 (DE-627)320421309 (DE-600)2002594-4 1466-1268 nnns volume:25 year:2019 number:1 day:19 month:11 pages:47-56 https://dx.doi.org/10.1007/s12192-019-01034-7 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_165 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_374 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_2018 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_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2019 1 19 11 47-56 |
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10.1007/s12192-019-01034-7 doi (DE-627)SPR025171623 (SPR)s12192-019-01034-7-e DE-627 ger DE-627 rakwb eng Feng, Yue verfasserin aut Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cell Stress Society International 2019 Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. Chicken liver (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Heat shock proteins (dpeaa)DE-He213 N6-methyladenosine (dpeaa)DE-He213 Hu, Yun aut Hou, Zhen aut Sun, Qinwei aut Jia, Yimin aut Zhao, Ruqian aut Enthalten in Cell stress & chaperones Dordrecht : Springer, 1996 25(2019), 1 vom: 19. Nov., Seite 47-56 (DE-627)320421309 (DE-600)2002594-4 1466-1268 nnns volume:25 year:2019 number:1 day:19 month:11 pages:47-56 https://dx.doi.org/10.1007/s12192-019-01034-7 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_165 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_374 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_2018 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_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2019 1 19 11 47-56 |
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10.1007/s12192-019-01034-7 doi (DE-627)SPR025171623 (SPR)s12192-019-01034-7-e DE-627 ger DE-627 rakwb eng Feng, Yue verfasserin aut Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cell Stress Society International 2019 Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. Chicken liver (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Heat shock proteins (dpeaa)DE-He213 N6-methyladenosine (dpeaa)DE-He213 Hu, Yun aut Hou, Zhen aut Sun, Qinwei aut Jia, Yimin aut Zhao, Ruqian aut Enthalten in Cell stress & chaperones Dordrecht : Springer, 1996 25(2019), 1 vom: 19. Nov., Seite 47-56 (DE-627)320421309 (DE-600)2002594-4 1466-1268 nnns volume:25 year:2019 number:1 day:19 month:11 pages:47-56 https://dx.doi.org/10.1007/s12192-019-01034-7 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_165 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_374 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_2018 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_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2019 1 19 11 47-56 |
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10.1007/s12192-019-01034-7 doi (DE-627)SPR025171623 (SPR)s12192-019-01034-7-e DE-627 ger DE-627 rakwb eng Feng, Yue verfasserin aut Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cell Stress Society International 2019 Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. Chicken liver (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Heat shock proteins (dpeaa)DE-He213 N6-methyladenosine (dpeaa)DE-He213 Hu, Yun aut Hou, Zhen aut Sun, Qinwei aut Jia, Yimin aut Zhao, Ruqian aut Enthalten in Cell stress & chaperones Dordrecht : Springer, 1996 25(2019), 1 vom: 19. Nov., Seite 47-56 (DE-627)320421309 (DE-600)2002594-4 1466-1268 nnns volume:25 year:2019 number:1 day:19 month:11 pages:47-56 https://dx.doi.org/10.1007/s12192-019-01034-7 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_165 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_374 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_2018 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_2939 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 25 2019 1 19 11 47-56 |
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English |
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Enthalten in Cell stress & chaperones 25(2019), 1 vom: 19. Nov., Seite 47-56 volume:25 year:2019 number:1 day:19 month:11 pages:47-56 |
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Enthalten in Cell stress & chaperones 25(2019), 1 vom: 19. Nov., Seite 47-56 volume:25 year:2019 number:1 day:19 month:11 pages:47-56 |
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Chicken liver Inflammation Fibrosis Heat shock proteins N6-methyladenosine |
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Feng, Yue @@aut@@ Hu, Yun @@aut@@ Hou, Zhen @@aut@@ Sun, Qinwei @@aut@@ Jia, Yimin @@aut@@ Zhao, Ruqian @@aut@@ |
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2019-11-19T00:00:00Z |
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In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. 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Feng, Yue |
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Feng, Yue misc Chicken liver misc Inflammation misc Fibrosis misc Heat shock proteins misc N6-methyladenosine Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken |
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Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken Chicken liver (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Heat shock proteins (dpeaa)DE-He213 N6-methyladenosine (dpeaa)DE-He213 |
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misc Chicken liver misc Inflammation misc Fibrosis misc Heat shock proteins misc N6-methyladenosine |
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Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken |
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Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken |
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Feng, Yue |
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10.1007/s12192-019-01034-7 |
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chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $a-linked post-transcriptional suppression of heat shock proteins in chicken |
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Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken |
| abstract |
Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. © Cell Stress Society International 2019 |
| abstractGer |
Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. © Cell Stress Society International 2019 |
| abstract_unstemmed |
Abstract Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with $ m^{6} $A-mediated post-transcriptional regulation. However, changes of HSPs and the $ m^{6} $A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, $ m^{6} $A methyltransferases METTL3 content was upregulated together with the level of $ m^{6} $A methylation on HSPs transcripts. The $ m^{6} $A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated $ m^{6} $A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated $ m^{6} $A peaks among which peaks on exon 16 and exon 17 showed 3.14- and 4.72-fold of increase, respectively. Mutation of the 8 predicted $ m^{6} $A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of $ m^{6} $A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens. © Cell Stress Society International 2019 |
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Chronic corticosterone exposure induces liver inflammation and fibrosis in association with $ m^{6} $A-linked post-transcriptional suppression of heat shock proteins in chicken |
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| score |
7.401025 |