RNA sequencing analysis of wild-type and Scd1-deficient CD4+ early iTregs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE224839 | GEO | 2023/02/13
REPOSITORIES: GEO
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Project description:Analysis of differentially expressed genes in Scd1-deficient CD4+ naïve T cells. The goal of this study was to elucidate the underlying pathway of Scd1-deficiency leading to increased regulatory T cell differentiation.
2023-08-28 | GSE160040 | GEO
Project description:To help elucidate the metabolic changes in the skin that contribute to the obesity resistance and skin pathology in mice lacking Scd1, we performed microarray analysis of skin gene expression in male skin Scd1 knockout (SKO) and Scd1 flox/flox control (Lox) mice fed a standard rodent diet. We identified an extraordinary number of differentially expressed genes that support the previously documented histological observations of sebocyte atrophy, inflammation and epidermal hyperplasia in SKO mice. Additionally, transcript levels were reduced in skin of SKO mice for genes involved in fatty acid synthesis, elongation and desaturation, which may be attributed to decreased abundance of key transcription factors including SREBP1c, ChREBP and LXR?. Conversely, genes involved in cholesterol synthesis were increased, suggesting an imbalance between skin fatty acid and cholesterol synthesis. Unexpectedly, we observed a robust elevation in skin retinol, retinoic acid and retinoic acid-induced genes in SKO mice. These results highlight the importance of monounsaturated fatty acid synthesis for maintaining retinol homeostasis and point to disturbed retinol metabolism as a novel contributor to the Scd1 deficiency-induced skin pathology. We analyzed dorsal skin gene expression in non-fasted 8-9 week old male skin Scd1 knockout (SKO) mice (n=3) and Scd1flox/flox (Lox) control mice (n=3)on a C57BL/6J background using Affymetrix 430 2.0 microarrays.
2011-05-09 | E-GEOD-24243 | biostudies-arrayexpress
Project description:To help elucidate the metabolic changes in the skin that contribute to the obesity resistance and skin pathology in mice lacking Scd1, we performed microarray analysis of skin gene expression in male skin Scd1 knockout (SKO) and Scd1 flox/flox control (Lox) mice fed a standard rodent diet. We identified an extraordinary number of differentially expressed genes that support the previously documented histological observations of sebocyte atrophy, inflammation and epidermal hyperplasia in SKO mice. Additionally, transcript levels were reduced in skin of SKO mice for genes involved in fatty acid synthesis, elongation and desaturation, which may be attributed to decreased abundance of key transcription factors including SREBP1c, ChREBP and LXRα. Conversely, genes involved in cholesterol synthesis were increased, suggesting an imbalance between skin fatty acid and cholesterol synthesis. Unexpectedly, we observed a robust elevation in skin retinol, retinoic acid and retinoic acid-induced genes in SKO mice. These results highlight the importance of monounsaturated fatty acid synthesis for maintaining retinol homeostasis and point to disturbed retinol metabolism as a novel contributor to the Scd1 deficiency-induced skin pathology.
2011-05-09 | GSE24243 | GEO
Project description:Thymus-originated tTregs and in vitro induced iTregs are subsets of regulatory T cells. While they share the capacity of immune suppression, their stabilities are different, with iTregs losing their phenotype upon stimulation or under inflammatory milieu. Epigenetic differences, particularly methylation state of Foxp3 CNS2 region, provide an explanation for this shift. Whether additional regulations, including cellular signaling, could directly lead phenotypical instability requires further analysis. Here we show that upon TCR triggering, store-operated calcium entry (SOCE) and NFAT nuclear translocation are blunted in tTregs, yet fully operational in iTregs, similar to Tconvs. On the other hand, tTregs show minimal changes in their chromatin accessibility upon activation, in contrast to iTregs that demonstrate an activated chromatin state with highly accessible T cell activation and inflammation related genes. Assisted by several cofactors, NFAT driven by strong SOCE signaling in iTregs preferentially binds to primed opened T helper (TH) genes, resulting in their activation normally observed only in Tconv activation, ultimately leads to instability. Conversely, suppression of SOCE in iTregs can partially rescue their phenotype. Thus our study adds two new layer, cellular signaling and chromatin accessibility, of understanding in Treg stability, and may provide a path for better clinical applications of Treg cell therapy.
2023-11-01 | GSE246431 | GEO
Project description:MBP TCR Tg mouse (1B3) generates only iTregs when crossed onto RAGKO background. Tregs from 1B3.RAG mouse were used for gene expression analsysis to determine genes selectively expressed in peripherally generated iTregs iTregs from 1B3.RAG mice (>90% Foxp3+) were run against total Tregs from 1B3 and WT NOD mice. Foxp3- CD4+T cells were used as control from all strains as Tconv. (1B3 denotes MBP-TCR Tg mouse).
2013-07-03 | E-GEOD-39724 | biostudies-arrayexpress
Project description:In this study, we have studied the genes associated with PRMT5 mediated histone methylation (H2R2me2s) in Th1-like iTregs. This particular epigenetic markers is upregulated in Th1 cells, and Th1-like iTregs. Therefore, we wanted to identify the genes H3R2me2s is regulating in Th1-like iTregs as compared to iTregs or Th1 cells. The goal of this sequencing was to identify if H2R2me2s is important for increased suppressive capacity of Th1-like iTregs or not.
2023-12-13 | GSE243686 | GEO
Project description:MBP TCR Tg mouse (1B3) generates only iTregs when crossed onto RAGKO background. Tregs from 1B3.RAG mouse were used for gene expression analsysis to determine genes selectively expressed in peripherally generated iTregs
2013-07-03 | GSE39724 | GEO
Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.
2017-08-01 | GSE98364 | GEO
Project description:Niche for stem cells can profoundly influence the position and fate of stem cells in tissue homeostasis and associated disorders, however, the mechanisms underlying the maintenance of stem cell niche remain poorly understood. Here we report that fatty acid desaturation catabolized by stearoyl-coenzyme A desaturase 1 (SCD1) regulates the activity of hair follicle stem cells (HFSCs) via blocking the formation of the bulge, a niche for HFSCs. We further unraveled that the abnormal hair growth in mice with SCD1 deletion is due to its function in K14+ basal keratinocytes rather than directly affecting HFSCs. Mechanistically, SCD1 deficiency impaired the expression of integrin α6 and the formation of hemidesmosomes (HDs), and thus allowed the activation of FAK in K14+ keratinocytes. Activated FAK subsequently stimulated PI3K and promoted the differentiation and proliferation of these keratinocytes, resulting in downward extension of the outer root sheath (ORS) and the disruption of bulge formation. Interestingly, inhibition of PI3K signaling restored bulge formation and normalized HFSCs and hair growth. Supplementation of oleic acid, the product of SCD1, to SCD1-/- mice also enhanced HD numbers, normalized the niche of HFSCs, and promoted hair growth in SCD1-/- mice. Taken together, SCD1 is indispensable for hair growth through stabilizing the number of HDs and thus sustaining bulge formation for HFSC residence and periodic activity.
2023-02-08 | GSE184346 | GEO
Project description:Purpose: To elucidate the effects of SCD1 inhibitor in allergic airway inflammation. Method: Wild-type mice were sensitized intratracheally twice with house dust mite (HDM) extract at a 7-day interval. Along with that, an SCD-1 inhibitor, A939572 was also administered intraperitoneally daily. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 385 transcripts showed differential expression between SCD1 inhibitor-treated mice and DMSO (vehicle)-treated mice with adjusted p value <0.05.
2022-04-01 | GSE190343 | GEO