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
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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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
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
author_sort guo, qiaoyan
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container_volume 2016
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