Se-methyselenocysteine inhibits inflammatory response in an LPS stimulated chicken HD11 macrophage-like cells model through the NFKB2 pathway
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ABSTRACT:
PROVIDER: PRJNA1165943 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30814542_1.fastq.gz | Fastqsanger.gz | |||
| SRR30814542_2.fastq.gz | Fastqsanger.gz | |||
| SRR30814543_1.fastq.gz | Fastqsanger.gz | |||
| SRR30814543_2.fastq.gz | Fastqsanger.gz | |||
| SRR30814544_1.fastq.gz | Fastqsanger.gz |
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Project description:Among the various sources of selenium supplementations, the Se-methylselenocysteine (SeMC) is a natural organic selenium compound that has been demonstrated to have multiple advantages in terms of metabolism efficiency and biosafety in animals. Nevertheless, the genome-wide impact of SeMC on gene transcription remains to be elucidated. In this study, we employed an LPS-stimulated chicken HD11 macrophage-like cell model to identify the principal transcription factors involved in transcriptome regulation responsible for SeMC treatment. RNA-seq identified 3,263 transcripts that exhibited a statistically significant differential expression between the SeMC-treated group and the control group and 1,344 transcripts that exhibited a statistically significant differential expression between the LPS + SeMC- and LPS-treated groups (FDR < 0.05, FDR > 1.5). The bioinformatic analysis identified six transcription factors (NFKB2, RFX2, E2F5, ETV5, BACH1, and E2F7) as potential candidate genes for transcriptome regulation in SeMC-treated HD11 cells. Subsequent experimental verification demonstrated that SeMC suppressed the inflammatory response in an LPS-stimulated chicken HD11 cell model via the TXN2-NF-κB pathway. The administration SeMC was observed to reduce the production of ROS as well as the transcription and translation of inflammatory cytokines in both cell culture and in vivo animal studies. One candidate pathway by which SeMC exerts its effects is through the targeting of the transcription factor, NFKB2, by selenoprotein TXN2. This study identified key transcription factors and revealed one of the potential mechanisms through which SeMC exerts its anti-inflammatory effects from the perspective of transcriptional regulation.
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Project description:The alternative (non-canonical) nuclear factor-kappa B (NF-κB) signalling pathway predominantly regulates the function of the p52/RelB heterodimer. Germline Nfkb2 deficiency in mice leads to loss of p100/p52 protein and offers protection against a variety of gastrointestinal conditions, such as azoxymethane/dextran sulfate sodium (DSS)-induced colitis-associated cancer and lipopolysaccharide (LPS)-induced small intestinal epithelial apoptosis. However, the common underlying protective mechanisms are not yet fully understood. Here we applied RNA sequencing and identified a B-lymphocyte defect as the major signature in the small intestinal mucosa of naïve adult Nfkb2-/- mice. Proteomics analysis also revealed a dramatic decrease in small intestinal immunoglobulin A levels, and this was validated by quantitative ELISA in both small intestinal lysates and serum. Moreover, the numbers of IgA-producing, CD138+ve plasma cells were also reduced in the lamina propria of the small intestinal villi of Nfkb2-/- mice. This phenotype was even more striking in the small intestinal mucosa of RelB-/- mice, although these mice were equally sensitive to LPS-induced intestinal apoptosis as their RelB+/+ wild-type counterparts. Therefore, p52 deficiency offers resistance to LPS-induced intestinal apoptosis and appears to regulate the plasma cell population within the gut.
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Project description:To investigate the effects of NFKB signaling, RNA-seq analysis was performed on both Jurkat and MT-2 cells. It was observed that either NFKB1 or NFKB2 knockout could alter the gene expression profile in MT-2 cells compared to Jurkat cells. Gene expression profiles of NFKB1/NFKB2 knockout Jurkat cells were compared to the mock edited Jurkat cells. On the other hand, it was hypothesized that the gene expression profile of MT-2 cells can be more drastically altered by NFKB1 or NFKB2 knockout. NFKB2 knockout MT-2 cells exhibited a unique gene expression profile compared to those of NFKB1 knockout MT-2 cells and mock edited MT-2 cells.
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Project description:As such, TNF triggers the canonical NF-?B pathway to induce a nuclear NF-?B activity composed of the RelA:p50 dimer in WT cells. Nfkb2 encodes p100, which regulates the activity of the RelB NF-?B heterodimers during immune cell-differentiation via the noncanonical pathway. Our biochemical analyses revealed that an absence of p100 instead repositions RelB under the control of the TNF-activated canonical pathway. Indeed, chronic TNF treatment of Nfkb2-/- cells activates the RelA:p50 dimer and an additional RelB:p50 dimer. On the other hand, TNF stimulation of Relb-/-Nfkb2-/- and Rela-/-Nfkb2-/- MEFs exclusively activated the RelA:p50 dimer and the RelB:p50 dimer, respectively. We treated this panel of knockout MEFs with TNF for 6h before being subjected to microarray mRNA analysis. We also included in our analysis WT MEFs and Rela-/-Relb-/-Rel-/- MEFs, which served as a negative control. Our analyses revealed overlapping and distinct gene-expression specificities of RelA:p50 and RelB:p50 dimers activated in mutant cells in response to TNF.
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