Genome-wide binding profile of Smad3 and Smad7 in mouse Ch12 cell line (ChIP-Seq)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA693862 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13500331.fastq.gz | Fastqsanger.gz | |||
| SRR13500332.fastq.gz | Fastqsanger.gz | |||
| SRR13500333.fastq.gz | Fastqsanger.gz | |||
| SRR13500334.fastq.gz | Fastqsanger.gz | |||
| SRR13500335.fastq.gz | Fastqsanger.gz |
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Project description:Genome-wide binding profile of Smad3 and Smad7 in mouse Ch12 cell line (RNA-Seq)
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Project description:Background: Abnormal autophagy and TGFβ-SMAD3/7 signaling pathway plays an important role in intrauterine adhesions (IUA); however, the exact underlying mechanisms remain unclear. In this study, we aimed to detect whether SMAD7 effected IUA via regulating autophagy and TGFβ-SMAD3 signaling pathway. Methods: The expression of p-SMAD3 and SMAD7 were detected by Immunohistochemistry. Endometrial fibrosis was detected by masson staining. The expression of protein related to autophagy and fibrosis was detected by western blot. The autophagic flux was monitored via Tandem mRFP-GFP-LC3 fluorescence system. Chip assay was used for SMAD3 binding site analysis. SMAD7 knockout mice were used to investigate the regulation of SMAD7 on intrauterine adhesions and autophagy. Results: we observed that patients with IUA exhibited a lower expression of SMAD7. In endometrial stromal cells, the silencing of SMAD7 inhibited autophagic flux, whereas overexpressed SMAD7 promoted autophagic flux. We also found that SMAD7-mediated autophagic flux regulated stromal-myofibroblast transition. These phenotypes are regulated by the transforming growth factor (TGF)β-SMAD3 signaling pathway. We found that SMAD3 directly binds to the 3ʹ-untranslated region of transcription factor EB (TFEB) and inhibits its transcription. SMAD7 promoted autophagic flux by inhibiting SMAD3, thereby promoting the expression of TFEB. The endometria of SMAD7 knockout mice showed a fibrotic phenotype. Simultaneously, autophagic flux was inhibited. On administering the autophagy activator rapamycin, endometrial fibrosis of SMAD7 gene conditional knockout mice was partially restored. Conclusions: The loss of SMAD7 promotes endometrial fibrosis by inhibited autophagic flux via the TGFβ-SMAD3 pathway. Therefore, this study reveals a potential therapeutic target for IUA.
2024-10-11 | GSE272824 | GEO
Project description:Forkhead box protein O3 (FOXO3) has good inhibition ability toward fibroblast activation and extracellular matrix, especially for the treatment of idiopathic pulmonary fibrosis. How FOXO3 regulates pulmonary fibrosis remains unclear. In this study, we reported that FOXO3 had binding sequences with F-spondin 1 (SPON1) promoter, which can activate its transcription and selectively promote the expression of SPON1 circRNA (circSPON1) but not mRNA expression. We further demonstrated that circSPON1 was involved in the extracellular matrix deposition of HFL1. In the cytoplasm, circSPON1 directly interacted with TGF-β-induced Smad3 and inhibited the activation of fibroblasts by inhibiting nuclear translocation. Moreover, circSPON1 bound to miR-942-5p and miR-520f-3p that interfered with Smad7 mRNA and promoted Smad7 expression. This study revealed the mechanism of FOXO3 in the occurrence and development of pulmonary fibrosis. Potential therapeutic targets and new insights into the diagnosis and treatment of idiopathic pulmonary fibrosis based on circRNA were also provided.
2021-09-10 | GSE183750 | GEO
Project description:Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.
2023-06-01 | GSE165281 | GEO
Project description:Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.
2023-06-01 | GSE165331 | GEO
Project description:Aging is an inevitable biological phenomenon that drives progressive functional decline at cellular and tissue levels, with chronic kidney disease (CKD) affecting up to 80% of cats over 15 years of age. Probiotic-derived metabolites hold anti-aging promise, but their renal protective mechanisms remain largely undefined. In this study, we investigated the anti-senescence effects of fermented brown algae extracts from Bifidobacterium adolescentis LA20-K9 (LA20FM) on feline kidney cells. Both the LA20FM<3 kDa and LA20FM>30 kDa molecular weight fractions mitigated doxorubicin-induced senescence, as evidenced by reduced SA-β-gal activity and decreased CDKN1A/CDKN2A expression. Peptide E, which was isolated from the LA20FM<3 kDa fraction, was identified as the principal bioactive component. RNA-sequencing revealed that peptide E downregulated senescence-associated genes, including IL6, CXCL8, GDF15, and KRT15, while upregulating the anti-senescence gene SMAD7. Mechanistically, peptide E enhanced SMAD7 expression, which in turn suppressed SMAD3 phosphorylation and consequently reduced IL6 and CXCL8 transcription. Crucially, SMAD7 knockdown completely abrogated these protective effects. Collectively, our findings identify peptide E as a novel bioactive peptide that antagonizes renal cellular senescence via the SMAD7/p-SMAD3/IL6-CXCL8 axis, offering a potential therapeutic candidate for age-related kidney dysfunction in felines.
2026-07-07 | GSE337653 | GEO
Project description:Cardiomyocytes are the major effectors of cardiac remodeling under pressure overload, undergoing hypertrophy and contractile dysfunction in response to sustained mechanical stress. These maladaptive changes are orchestrated by transforming growth factor beta (TGF-β), a key mediator of hypertrophic and profibrotic signaling. Smad7, an inhibitory Smad, negatively regulates TGF-β signaling, but its cardiomyocyte-specific role in pathological remodeling is unclear. We hypothesized that Smad7 acts as an endogenous inhibitor of cardiomyocyte dysfunction during pressure overload. To investigate this, we generated cardiomyocyte-specific Smad7 knockout (CMS7KO) mice and subjected them to transverse aortic constriction (TAC). Echocardiography, RNA-sequencing, histological, and molecular analyses were performed. Smad7 expression was upregulated in cardiomyocytes of TAC mouse hearts and in patients with non-ischemic cardiomyopathy. While baseline cardiac function was preserved in CMS7KO mice, TAC induced an increase in systolic and diastolic dysfunction, ventricular dilation, and hypertrophy compared to controls. Histological analysis revealed increased cardiomyocyte size and macrophage infiltration, without significant fibrosis. Transcriptomic profiling showed downregulation of contractile and sarcomeric genes. Cardiomyocyte-specific Smad7 loss enhanced TGF-β/Smad3 and ERBB2 signaling in vivo. In H9c2 cardiomyocyte-like cells, Smad7 knockdown increased TbR1 and Smad3 phosphorylation, confirming a direct inhibitory effect. These findings identify cardiomyocyte Smad7 as a critical regulator of pathological remodeling and a potential therapeutic target in heart failure.
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Project description:We report that nuclear PTEN negatively regulates DNA-binding activity of SMAD3. We compared SMAD3 binding activity in colorectal tumor cells without or with a nuclear PTEN (C124S) mutant.
2020-12-31 | GSE109956 | GEO
Project description:Cardiomyocytes are the major effectors of cardiac remodeling under pressure overload, undergoing hypertrophy and contractile dysfunction in response to sustained mechanical stress. These maladaptive changes are orchestrated by transforming growth factor beta (TGF-β), a key mediator of hypertrophic and profibrotic signaling. Smad7, an inhibitory Smad, negatively regulates TGF-β signaling, but its cardiomyocyte-specific role in pathological remodeling is unclear. We hypothesized that Smad7 acts as an endogenous inhibitor of cardiomyocyte dysfunction during pressure overload. To investigate this, we generated cardiomyocyte-specific Smad7 knockout (CMS7KO) mice and subjected them to transverse aortic constriction (TAC). Echocardiography, RNA-sequencing, histological, and molecular analyses were performed. Smad7 expression was upregulated in cardiomyocytes of TAC mouse hearts and in patients with non-ischemic cardiomyopathy. While baseline cardiac function was preserved in CMS7KO mice, TAC induced an increase in systolic and diastolic dysfunction, ventricular dilation, and hypertrophy compared to controls. Histological analysis revealed increased cardiomyocyte size and macrophage infiltration, without significant fibrosis. Transcriptomic profiling showed downregulation of contractile and sarcomeric genes. Cardiomyocyte-specific Smad7 loss enhanced TGF-β/Smad3 and ERBB2 signaling in vivo. In H9c2 cardiomyocyte-like cells, Smad7 knockdown increased TbR1 and Smad3 phosphorylation, confirming a direct inhibitory effect. These findings identify cardiomyocyte Smad7 as a critical regulator of pathological remodeling and a potential therapeutic target in heart failure.
2026-06-06 | GSE299359 | GEO
Project description:The aim of this study is to identify SMAD3 binding targets affected by the TGFb1/SMAD3 signal transduction on a genome-wide scale
2011-06-01 | GSE28346 | GEO