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TGF-β/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-Differentiation

ABSTRACT: In order to determine a mechanism through which TGF-b/Smad3 promote these effects, Affymetrix gene expression arrays were performed on primary rat SMCs infected with Smad3 and stimulated with TGF-b or infected with GFP alone. More than 200 genes were differentially expressed (>2.0 fold change, p<0.05) in TGF-b/Smad3 stimulated SMCs. We then performed GO term enrichment analysis using the DAVID bioinformatics database and found that TGF-b/Smad3 activated the expression of multiple genes related to either development or cell differentiation, several of which have been shown to be associated with multipotent stem or progenitor cells.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE54624 | GEO | 2014/02/04

SECONDARY ACCESSION(S): PRJNA237211

REPOSITORIES: GEO

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TGF-Î²/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-Differentiation

Project description:In order to determine a mechanism through which TGF-b/Smad3 promote these effects, Affymetrix gene expression arrays were performed on primary rat SMCs infected with Smad3 and stimulated with TGF-b or infected with GFP alone. More than 200 genes were differentially expressed (>2.0 fold change, p<0.05) in TGF-b/Smad3 stimulated SMCs. We then performed GO term enrichment analysis using the DAVID bioinformatics database and found that TGF-b/Smad3 activated the expression of multiple genes related to either development or cell differentiation, several of which have been shown to be associated with multipotent stem or progenitor cells. Vascular smooth muscle cells from 3 rats were infected with adenovirus expressing Smad3 and treated with TGF-B for 24 h (TGF-B/Smad3 group). Adenovirus expressing GFP (GFP group) was control. TGF-B/Smad3 treated or control cells were used for RNA extraction and hybridization on Affymetrix microarrays (n=3).

2014-02-04 | E-GEOD-54624 | biostudies-arrayexpress

Protection from obesity and diabetes by blockade of TGF-beta/Smad3 signaling

Project description:Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-beta/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3 deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3-/- white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3-/- adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-alpha1 expression. We observe significant correlation between TGF-beta1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-beta1 signaling protects mice from obesity, diabetes and hepatic steatosis. Together, these results demonstrate that TGF-beta signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-beta1 activity might be an effective treatment strategy for obesity and diabetes. Smad3-/- and WT mice were fed with regular diet (RD) and high fat diet (HFD), and diet induced obese (DIO) mice were treated with IgG and anti-TGF-b1 antibody

2011-07-12 | E-GEOD-28598 | biostudies-arrayexpress

TGF-beta/Smad3-dependent gene expression analysis in naive CD4 T cells

Project description:Investigation of transcript level modulation in unstimulated and TGF-beta treated (with or without superimposed T-cell receptor and CD28 stimulation) naive CD4 T cells from wild type or Smad3-deficient littermate mice. Smad3 is a critical signaling molecule and transcription factor downstream of TGF-beta and mediates several of the TGF-beta dependent tolerogenic effects in T cells. This study was undertaken to unveil the transcriptionnal program controled by the TGF-b/Smad3 axis. Microarray study using RNA recovered after 6 hours of culture in either serum free media, serum-free media + TGF-beta (2.5ng/ml) or serum-free media + TGF-beta and anti-CD3e and anti-CD28 stimulation (3 conditions). Naive CD4 T cells (TCRb+, CD4+, CD62L+ and CD44-) were sorted from either wild type or Smad3 deficient littermates and submitted to the 3 culture conditions. Three biological replicates were obtained (each from at least 2 different mice). Thus a total of 18 Nimblegen 365K chip were used.

2012-08-31 | E-GEOD-40494 | biostudies-arrayexpress

TGF-beta/Smad3-dependent gene expression analysis in naive CD4 T cells

2012-08-31 | GSE40494 | GEO

Protection from obesity and diabetes by blockade of TGF-beta/Smad3 signaling

2011-07-13 | GSE28598 | GEO

SMAD3 targets in A549 lung epithelial cells

Project description:TGF? activates a signal transduction cascade that results in the transcription of genes, primarily through the DNA-binding transcription factor SMAD3. The objective of this study is to identify SMAD3 binding targets and the molecular pathways affected by the TGF?1/SMAD3 signal transduction on a genome-wide scale. Cultured A549 cells at 30-50% confluence were treated with 10 uM SIS3 in dimethyl sulfoxide (DMSO), or DMSO (vehicle-only) 30 min prior to TGF?1 treatment. Cells were treated with 2 ng/mL recombinant TGF?1 for 0, 2, 12, and 24 h.

2011-06-24 | E-GEOD-26858 | biostudies-arrayexpress

Expression data from C2C12 cells with or without Smad3 overexpression

Project description:The goal of this study was to identify genes in C2C12 myoblasts whose expression was altered by overexpression of Smad3. Four total samples were analyzed. Two biological replicates were prepared from C2C12 cells infected with retroviral vector encoding wildtype Smad3 and exposed for 24 hours to 100 pM TGF-β. Two biological replicates were prepared from C2C12 cells infected with a control retrovirus that did not encode Smad3 (empty vector, EV) and exposed for 24 hours to 100pM TGF-β. To identify genes with altered expression between empty vector controls and cells overexpressing wild-type Smad3, we first pre-processed the four arrays using robust multiarray averaging as implemented in the R software package ‘xps’, version 1.10.2 (http://www.bioconductor.org/packages/release/bioc/html/xps.html). This preprocessing corrects for background noise and array effects, and aggregates probe data to 28,836 genes. Duplicates were averaged on the base-2 logarithm scale, and then we took differences between the averages to obtain logarithm-scale fold changes. Genes were selected which showed at least a two-fold change (raw scale) between wild-type and empty vector expressing cells. Due to the limited sample size, we did not apply any statistical tests to estimate false-discovery rate. This resulted in 79 genes that were at least two-fold higher in the wild-type Smad3-expressing C2C12 cells compared to empty vector cells and 25 genes that were at least two-fold lower in the wild-type Smad3-expressing cells than the in the empty vector cells.

2011-10-20 | E-GEOD-30459 | biostudies-arrayexpress

Identification of genes associated with TGF-beta/Smad3-mediated macrophage-myofibroblast transition (MMT) by single-cell RNA sequencing

Project description:In this study, we conducted single-cell RNA sequencing (scRNA-Seq) to identify the Smad3-dependent transcriptomes related to MMT in TGF-beta1-treated bone marrow-derived macrophages in vitro, where Smad3-KO group serves as a negative control.

2018-07-01 | GSE100706 | GEO

Long noncoding RNA ELIT-1 acts as a Smad3 cofactor to facilitate TGF-β/Smad signaling and promote epithelial-mesenchymal transition

Project description:TGF-β is involved in various biological processes, including development, differentiation, growth regulation, and epithelial-mesenchymal transition (EMT). In TGF-β/Smad signaling, receptor-activated Smad complexes activate or repress their target gene promoters. Smad cofactors are a group of Smad-binding proteins that promote recruitment of Smad complexes to these promoters. Long noncoding RNAs (lncRNAs), that behave as Smad cofactors have thus far not been identified. Here, we characterize a novel lncRNA EMT-associated lncRNA induced by TGF-β-1(ELIT-1). ELIT-1 was induced by TGF-β-stimulation via the TGF-β/Smad pathway in TGF-β-responsive cell lines. ELIT-1-depletion abrogated TGF-β-mediated EMT progression and expression of TGF-β target genes including Snail, a transcription factor critical for EMT. A positive correlation between high expression of ELIT-1 and poor prognosis in lung adenocarcinoma and gastric cancer patients suggests that ELIT-1 may be useful as a prognostic and therapeutic target. RIP assays revealed that ELIT-1 bound to Smad3, but not Smad2. In conjunction with Smad3, ELIT-1 enhanced Smad-responsive promoter activities by recruiting Smad3 to the promoters of its target genes including Snail, other TGF-β-target genes, and ELIT-1 itself. Collectively, these data show that ELIT-1 is a novel trans-acting lncRNA that forms a positive feedback loop to enhance TGF-β/Smad3 signaling and promote EMT progression.

2019-04-12 | GSE129008 | GEO

Long noncoding RNA ELIT-1 acts as a Smad3 cofactor to facilitate TGF-β/Smad signaling and promote epithelial-mesenchymal transition

2019-04-12 | GSE128965 | GEO

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