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Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells
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Zeitschriftentitel: | BioMed Research International |
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Personen und Körperschaften: | , , , , , , |
In: | BioMed Research International, 2016, 2016, S. 1-9 |
Format: | E-Article |
Sprache: | Englisch |
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Hindawi Limited
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author_facet |
Guo, Qiaoyan Li, Xiaoxia Han, Hongbo Li, Chaoyuan Liu, Shujun Gao, Wenhui Sun, Guangdong Guo, Qiaoyan Li, Xiaoxia Han, Hongbo Li, Chaoyuan Liu, Shujun Gao, Wenhui Sun, Guangdong |
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author |
Guo, Qiaoyan Li, Xiaoxia Han, Hongbo Li, Chaoyuan Liu, Shujun Gao, Wenhui Sun, Guangdong |
spellingShingle |
Guo, Qiaoyan Li, Xiaoxia Han, Hongbo Li, Chaoyuan Liu, Shujun Gao, Wenhui Sun, Guangdong BioMed Research International Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine |
author_sort |
guo, qiaoyan |
spelling |
Guo, Qiaoyan Li, Xiaoxia Han, Hongbo Li, Chaoyuan Liu, Shujun Gao, Wenhui Sun, Guangdong 2314-6133 2314-6141 Hindawi Limited General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine http://dx.doi.org/10.1155/2016/6927234 <jats:p>Transforming growth factor beta1- (TGF-<jats:italic>β</jats:italic>1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-<jats:italic>β</jats:italic>1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-<jats:italic>β</jats:italic>1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-<jats:italic>β</jats:italic>1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.</jats:p> Histone Lysine Methylation in TGF-<i>β</i>1 Mediated p21 Gene Expression in Rat Mesangial Cells BioMed Research International |
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10.1155/2016/6927234 |
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title |
Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_unstemmed |
Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_full |
Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_fullStr |
Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_full_unstemmed |
Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_short |
Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_sort |
histone lysine methylation in tgf-<i>β</i>1 mediated p21 gene expression in rat mesangial cells |
topic |
General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine |
url |
http://dx.doi.org/10.1155/2016/6927234 |
publishDate |
2016 |
physical |
1-9 |
description |
<jats:p>Transforming growth factor beta1- (TGF-<jats:italic>β</jats:italic>1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-<jats:italic>β</jats:italic>1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-<jats:italic>β</jats:italic>1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-<jats:italic>β</jats:italic>1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.</jats:p> |
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author | Guo, Qiaoyan, Li, Xiaoxia, Han, Hongbo, Li, Chaoyuan, Liu, Shujun, Gao, Wenhui, Sun, Guangdong |
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author_sort | guo, qiaoyan |
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description | <jats:p>Transforming growth factor beta1- (TGF-<jats:italic>β</jats:italic>1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-<jats:italic>β</jats:italic>1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-<jats:italic>β</jats:italic>1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-<jats:italic>β</jats:italic>1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.</jats:p> |
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spelling | Guo, Qiaoyan Li, Xiaoxia Han, Hongbo Li, Chaoyuan Liu, Shujun Gao, Wenhui Sun, Guangdong 2314-6133 2314-6141 Hindawi Limited General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine http://dx.doi.org/10.1155/2016/6927234 <jats:p>Transforming growth factor beta1- (TGF-<jats:italic>β</jats:italic>1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-<jats:italic>β</jats:italic>1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-<jats:italic>β</jats:italic>1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-<jats:italic>β</jats:italic>1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-<jats:italic>β</jats:italic>1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.</jats:p> Histone Lysine Methylation in TGF-<i>β</i>1 Mediated p21 Gene Expression in Rat Mesangial Cells BioMed Research International |
spellingShingle | Guo, Qiaoyan, Li, Xiaoxia, Han, Hongbo, Li, Chaoyuan, Liu, Shujun, Gao, Wenhui, Sun, Guangdong, BioMed Research International, Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells, General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine |
title | Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_full | Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_fullStr | Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_full_unstemmed | Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_short | Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
title_sort | histone lysine methylation in tgf-<i>β</i>1 mediated p21 gene expression in rat mesangial cells |
title_unstemmed | Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells |
topic | General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine |
url | http://dx.doi.org/10.1155/2016/6927234 |