IndraLab
Statements
"Peripheral blood mononuclear cells of patients with COPD have decreased telomere length, a hallmark of senescing cells in vitro, when compared with normal individuals (225). This observation has been extended to lung cells, as alveolar epithelial and endothelial cells of emphysema patients exhibited enhanced expression of markers of cell senescence including p16Ink4a and p21CIP1/WAF1/Sdi1 and telomere shortening when compared with smokers without emphysema and normal individuals (320).TGF-beta1 played a role in the upregulation of p21CIP1/WAF1/Sdi1 in the alveolar type II-like epithelial cell line A549 (205). "
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"In the present report, firstly we confirmed that TGF-beta1 treatment could upregulate p21 gene expression in RMC; then we found significant changes of histone lysine methylations, including H3K9me2/3 and H3K4me1/2/3 levels at p21 gene promoter, which were closely associated with p21 gene expression; further results showed that SET7/9, the specific H3K4me1 HMT, was involved in TGF-beta1 induced p21 gene upregulation in RMC."
"Therefore, we decided to address the role of miR-106b-25 in the presence of TGFb: this cytokine, by inducing the expression of p21 and other antiproliferative molecules, ensures timely coordinated cell-cycle arrest and apoptosis of mature cells in the gastrointestinal tract, thus controlling the physiological turnover of epithelial cells (van den Brink and Offerhaus, 2007)."
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"To further understand the key roles of H3K4me in regulating TGF-beta1-induced p21 expression, we investigated the levels of H3K4me1/2/3 in RMC exposed to TGF-beta1 for 24h; subsequently our current results showed that TGF-beta1 upregulated p21 gene expression in RMC, which is positively correlative with the increased H3K4me1/2/3 levels at the p21 promoter."
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"Although the known TbetaRIII ligands, BMP-2, BMP-4, and TGFbeta-1, also increased p21 and p27 expression (XREF_FIG), the magnitude of increase was similar in the presence and absence of TbetaRIII, suggesting that, consistent with the proliferation data, the effects of TbetaRIII are largely independent of its ligand presentation role."
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"Our results indicated that TGF-beta1 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 and H3K9me3) at p21 gene promoter."
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"In that vein, we previously demonstrated that both Activin A and TGFbeta1 signal via SMAD dependent pathways to up-regulate expression of the cell cycle inhibitor p21 at early time points and further identified p21 as a predictor of net upstream Activin A and TGFbeta1 pathway signaling both in vitro and in patient samples 15."
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"The Rac1b siRNA mediated relief from inhibition of ERK signaling might account for Rac1b siRNA induced increase in TGF-beta1 induction of p21 WAF1 expression since p21 WAF1 is upregulated by TGF-beta and Smad and MEK-ERK signaling in an oxidative stress and ROS dependent manner [XREF_BIBR, XREF_BIBR]."
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"We found that the expression of cyclin A and p21 (WAF1) molecules was primarily modulated by TGFbeta1 treatment while the expression of other regulatory components, like cyclins D, cyclin E, cdk2, cdk4, and cdk6 or p15 (INK4B), p16 (INK4A), and p27 (KIP1) was not significantly affected."