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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [CUT&RUN]

ABSTRACT: In this study, we define the epithelial-specific contribution of SMAD2/3 to endometrial function by conditionally ablating the Smad2 and Smad3 transcription factors using Lactoferrin-iCre (Ltf-cre). Using epithelial organoid cultures from the endometrium, we uncover the signaling mechanisms downstream of TGFβ that control endometrial cell regeneration and are critical for endometrial regeneration and homeostasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE212474 | GEO | 2023/01/30

REPOSITORIES: GEO

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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [RNA-Seq]

Project description:In this study, we define the epithelial-specific contribution of SMAD2/3 to endometrial function by conditionally ablating the Smad2 and Smad3 transcription factors using Lactoferrin-iCre (Ltf-cre). Using epithelial organoid cultures from the endometrium, we uncover the signaling mechanisms downstream of TGFβ that control endometrial cell regeneration and are critical for endometrial regeneration and homeostasis.

2023-01-30 | GSE212475 | GEO

Expression data for nasopharyngeal carcinoma cell line 5-8F stably expressing either LTF gene or empty vector.

Project description:LTF (lactotransferrin, lactoferrin) is a key component of innate immune defense. It has recently been found to have antitumor and antimetastatic activity in different cancers. We previously reported LTF to be the most significantly downregulated gene in nasopharyngeal carcinoma (NPC) specimens relative to normal nasopharyngeal epithelial tissues and it was also negatively associated with the progression and metastasis of NPC. However, the mechanism underlying this remains unclear. In the current study, we performed genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with LTF gene overexpression in NPC cell line 5-8F. NPC cell line5-8F were transfected with either PIRES empty vector (Clontech) or PIRES-LTF vector by Lipofectamine 2000 (Invitrogen). Cells stably expressing either LTF or empty vector were generated by selection with growth medium supplemented with 400 M-NM-<g/mL G418. When cells were growing at 80% confluence, total RNA were extracted and detected by Affymerix GeneChip Human Gene U133 plus2.0.

2013-12-26 | E-GEOD-36972 | biostudies-arrayexpress

RNAi profiling by array of of Smad2 and Smad3 in mouse mammary epithelial cells treated with TGF-beta to induce epithelial-to-mesenchymal transition

Project description:Effects of Smad3 and Smad2 knock-down on TGFbeta-induced epithelial-to-mesenchymal transition (EMT) in mouse mammary epithelial (Nme) cells

2009-04-01 | E-MEXP-1342 | biostudies-arrayexpress

Expression data for nasopharyngeal carcinoma cell line 5-8F stably expressing either LTF gene or empty vector.

2013-12-26 | GSE36972 | GEO

Smad2 and Smad3 have differential sensitivity in relaying TGF b signaling and inversely regulate early lineage specification

Project description:The transforming growth factor beta (TGFÎ²) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 are structurally similar and it is mostly considered that they are equally important in mediating TGFÎ² signals. Here, we show that Smad3 is an insensitive TGFÎ² transducer as compared with Smad2. Smad3 preferentially localizes within the nucleus and is thus sequestered from membrane signaling. The ability of Smad3 in oligomerization with Smad4 upon agonist stimulation is also impaired given its unique linker region. Smad2 mediated TGFÎ² signaling plays a crucial role in epiblast development and patterning of three germ layers. However, signaling unrelated nuclear localized Smad3 is dispensable for TGFÎ² signaling-mediated epiblast specification, but important for early neural development, an event blocked by TGFÎ²/Smad2 signaling. Both Smad2 and Smad3 bind to the conserved Smads binding element (SBE), but they show nonoverlapped target gene binding specificity. We conclude that Smad2 and Smad3 possess differential sensitivities in relaying TGFÎ² signaling and have distinct roles in regulating early developmental events. GFP, GFP-Smad2 and GFP-Smad3 constitutively expressed Smad3-/- mouse ESCs were differentiated to day6 neuroepithelia and collected for Chip-Seq with an anti-GFP antibody.

2016-03-01 | E-GEOD-76557 | biostudies-arrayexpress

Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium

Project description:TGF-βs regulate macrophage responses, by activating Smad2/3. We have previously demonstrated that macrophage-specific Smad3 stimulates phagocytosis and mediates anti-inflammatory macrophage transition in the infarcted heart. However, the role of macrophage Smad2 signaling in myocardial infarction remains unknown. We studied the role of macrophage-specific Smad2 signaling in the healing infarct, and we explored the basis for the distinct effects of Smad2 and Smad3. Infarct macrophages exhibited both Smad2 and Smad3 activation. In contrast to the effects of Smad3 loss, myeloid cell-specific Smad2 disruption had no effects on mortality, ventricular dysfunction and adverse remodeling, after myocardial infarction. Phagocytic removal of dead cells, macrophage and myofibroblast infiltration, collagen deposition, angiogenesis and scar remodeling were not affected by macrophage Smad2 loss. In isolated macrophages, TGF-β1, -β2 and -β3, activated both Smad2 and Smad3, whereas BMP6 triggered only Smad3 activation. Smad2 and Smad3 had similar patterns of nuclear translocation in response to TGF-β1. Smad3, and not Smad2, was the main mediator of transcriptional effects of TGF-β on macrophages and Smad3 loss resulted in enrichment of genes associated with RAR/RXR signaling, cholesterol biosynthesis and lipid metabolism. In conclusion, the in vivo and in vitro effects of TGF-β on macrophage function involve Smad3, and not Smad2.

2022-04-29 | GSE185634 | GEO

Smad2 and Smad3 binding sites in H345-TbRII cells

Project description:Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta. Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).

2015-09-15 | E-GEOD-63871 | biostudies-arrayexpress

Gene expression profiling of Smad2/3 cKO mice

Project description:Uterine double conditional inactivation of Smad2 and Smad3 in mice results in endometrial dysregulation, infertility, and uterine cancer. Smad2/3 cKO mice demonstrate abnormal expression of genes involved in inflammation, cell-cycle checkpoint, migration, steroid biosynthesis, and SMAD1/5-driven genes. We performed RNA-sequencing to identify the gene expression differences between the uterine epithelium of control and Smad2/3 cKO. To control for estrous cycle variations, the uterine epithelium was collected from mice at 0.5 dpc. Global gene expression profiles of Smad2/3 cKO versus control mice was analyzed. Our RNA sequencing analysis was performed at 6 weeks of life and already showed significant differences in migratory (Agr2,Slit2) and inflammatory (Ccl20, Crispld2) markers between Smad2/3 cKO and control mice.

2019-03-12 | GSE112664 | GEO

Smad2 and Smad3 have differential sensitivity in relaying TGF b signaling and inversely regulate early lineage specification

Project description:The transforming growth factor beta (TGFβ) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 are structurally similar and it is mostly considered that they are equally important in mediating TGFβ signals. Here, we show that Smad3 is an insensitive TGFβ transducer as compared with Smad2. Smad3 preferentially localizes within the nucleus and is thus sequestered from membrane signaling. The ability of Smad3 in oligomerization with Smad4 upon agonist stimulation is also impaired given its unique linker region. Smad2 mediated TGFβ signaling plays a crucial role in epiblast development and patterning of three germ layers. However, signaling unrelated nuclear localized Smad3 is dispensable for TGFβ signaling-mediated epiblast specification, but important for early neural development, an event blocked by TGFβ/Smad2 signaling. Both Smad2 and Smad3 bind to the conserved Smads binding element (SBE), but they show nonoverlapped target gene binding specificity. We conclude that Smad2 and Smad3 possess differential sensitivities in relaying TGFβ signaling and have distinct roles in regulating early developmental events.

2016-03-01 | GSE76557 | GEO

The phosphorylation of the Smad2/3 linker region by Nemo-like kinase regulates TGF-β signaling

Project description:Smad2 and Smad3 (Smad2/3) primarily mediates the transforming growth factor-β (TGF-β) signaling that drives cell proliferation, differentiation, and migration. The dynamics of the Smad2/3 phosphorylation provides the key mechanism for regulating the TGF-β signaling pathway. Here we identified NLK as a novel regulator of TGF-β signaling pathway via modulating the phosphorylation of Smad2/3 in the linker region.

2021-09-10 | PXD023957 | Pride

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