Effect of ablation of CEACAM1 on gene expression in human regulatory T cells
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PROVIDER: PRJNA1080673 | ENA |
REPOSITORIES: ENA
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Project description:To study the contribution of CEACAM1 in human Tregs, CEACAM1 was knocked out in ex-vivo expanded human Tregs by Crispr/Cas9. Tregs transfected with scramble gRNAs were used as controls. After electroporation, scramble or CEACAM1KO Tregs were subcultured with IL-2 for 7 days and RNA was isolated for genome-wide RNA-seq. Gene expression profiling analysis was performed using data obtained from RNA-seq of two replicates of CEACAM1KO and control cells.
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Project description:Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at the various developmental stages before, during, and after palate fusion using GeneChip? microarrays. Ceacam1 was one of the highly up-regulated genes during and after fusion in palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was expressed at a very low level in palatal epithelium before fusion, but highly expressed in the midline of the palate during and after fusion. To investigate the developmental role of CEACAM1, function-blocking antibody was added to embryonic mouse palate in organ culture. Palatal fusion was inhibited by this function-blocking antibody. To investigate the subsequent developmental role of CEACAM1, we characterized Ceacam1-deficient (Ceacam1-/-) mice. Epithelial cells persisted abnormally at the midline of the embryonic palate even on day E16.0, and palatal fusion was delayed in Ceacam1-/- mice. TGF?3 expression, apoptosis, and cell proliferation in palatal epithelium were not effected in the palate of Ceacam1-/-mice. CEACAM1 expression was down-regulated in Tgfb3-/- palate. However, exogenous TGF?3 did not induce CEACAM1 expression. These results suggest that CEACAM1 has roles in both the initiation of palate formation via epithelial cell adhesion and TGF signaling has some indirect effect on CEACAM1. Global gene expression profiling of palatal processes before, during and after fusion of palatal shelves We used microarray to investigate the gene expression of palatal tissue during palatal development. Palatal processes were microdissected at the stages of palatal development (before, during and after fusion) for RNA extraction and hybridization on Affymetrix microarrays.
2013-01-23 | E-GEOD-43651 | biostudies-arrayexpress
Project description:Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at the various developmental stages before, during, and after palate fusion using GeneChip? microarrays. Ceacam1 was one of the highly up-regulated genes during and after fusion in palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was expressed at a very low level in palatal epithelium before fusion, but highly expressed in the midline of the palate during and after fusion. To investigate the developmental role of CEACAM1, function-blocking antibody was added to embryonic mouse palate in organ culture. Palatal fusion was inhibited by this function-blocking antibody. To investigate the subsequent developmental role of CEACAM1, we characterized Ceacam1-deficient (Ceacam1-/-) mice. Epithelial cells persisted abnormally at the midline of the embryonic palate even on day E16.0, and palatal fusion was delayed in Ceacam1-/- mice. TGF?3 expression, apoptosis, and cell proliferation in palatal epithelium were not effected in the palate of Ceacam1-/-mice. CEACAM1 expression was down-regulated in Tgfb3-/- palate. However, exogenous TGF?3 did not induce CEACAM1 expression. These results suggest that CEACAM1 has roles in both the initiation of palate formation via epithelial cell adhesion and TGF signaling has some indirect effect on CEACAM1. Global gene expression profiling of palatal processes before, during and after fusion of palatal shelves We used microarray to investigate the gene expression of palatal tissue during palatal development.
2013-01-23 | GSE43651 | GEO
Project description:To identify Ceacam1 downstream factors, we compared gene expressions between NSCs and Ceacam1L-expressing NSC and between NSCL61 and Ceacam1shRNA-expressing NSCL61. We established Ceacam1L-expressing NSC and Ceacam1shRNA-expressing NSCL61s. We think that genes, which are differently expressed between NSC and Ceacam1L-NSC, and between NSCL61 and Ceacam1shRNA-NSCL61, are the Ceacam1 downstream factors.
2015-11-04 | E-GEOD-70023 | biostudies-arrayexpress
Project description:Identification of genes involved in lumen formation: gene chip analysis was performed on mRNA isolated from both wild type and T457A,S459A mutated CEACAM1-4S transfected MCF7 cells grown in Matrigel Experiment Overall Design: Microarray analysis of RNA isolated from MCF7 cells transfected with CEACAM1-S wild-type (SW) or CEACAM1-S double-A mutant T457A,S459A (DA) grown in Matrigel for 4 days
2009-10-10 | E-GEOD-17540 | biostudies-arrayexpress
Project description:Mesenchymal stem cells (MSCs) have garnered attention for their regenerative and immunomodulatory capabilities in clinical trials for various diseases. However, the effectiveness of MSC-based therapies, especially for conditions like graft-versus-host disease (GvHD), remains uncertain. The cytokine IFN-γ has been known to enhance the immunosuppressive properties of MSCs through cell-to-cell interactions and soluble factors. In this study, we observed that IFN-γ-treated MSCs upregulated the expression of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), associated with immune evasion through the inhibition of NK cell cytotoxicity. To co-opt this immunomodulatory function, we generated MSCs overexpressing CEACAM1 and found that CEACAM1-engineered MSCs significantly reduced NK cell activation and cytotoxicity, independent of NKG2D ligand regulation. Furthermore, CEACAM1-engineered MSCs effectively inhibited the proliferation and activation of T cells along with the inflammatory responses of monocytes. In a humanized GvHD mouse model, CEACAM1-MSCs, particularly CEACAM1-4S-MSCs, demonstrated therapeutic potential by improving survival and alleviating symptoms. These findings suggest that CEACAM1 expression on MSCs contributes to MSC-mediated regulation of immune responses and that CEACAM1-engineered MSC could have therapeutic potential in conditions involving immune dysregulation.
2024-11-03 | GSE262974 | GEO
Project description:To identify Ceacam1 downstream factors, we compared gene expressions between NSCs and Ceacam1L-expressing NSC and between NSCL61 and Ceacam1shRNA-expressing NSCL61.
2015-11-04 | GSE70023 | GEO