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Effect of Bmal1 depletion on gene expression in poly(I:C)-stimulated myeloid peritoneal cells.

ABSTRACT: To investigate the effect of Bmal1 on poly(I:C) response, we isolate mRNA from PBS or poly(I:C)-injected WT and myeloid Bmal1 KO mice. We then compare the poly(I:C)-induced transcriptomic change between WT and Bmal1 KO peritoneal myeloid cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE222759 | GEO | 2024/01/31

REPOSITORIES: GEO

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Genome-wide analysis of LPS or PBS challenged DUSP3-KO and WT female mice peritoneal macrophages gene expression

Project description:Analysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions. Total RNA obtained from isolated peritoneal macrophages isolated from DUSP3-/- and WT mice 36 hours after challenging them in vivo with PBS or with 6mg/kg of LPS.

2015-03-11 | E-GEOD-66782 | biostudies-arrayexpress

Genome-wide analysis of LPS or PBS challenged DUSP3-KO and WT female mice peritoneal macrophages gene expression

2015-03-11 | GSE66782 | GEO

Differential gene expression in mice with inducible loss of Bmal1 and HNF4α in the liver

Project description:Hepatocyte Nuclear Factor 4 alpha (HNF4α), a master regulator of hepatocyte differentiation, and circadian regulator Aryl Hydrocarbon-Like Receptor-Like 1 (ARNTL, or BMAL1) though robustly co-expressed in healthy liver, are incompatible within the context of HCC. Differential expression of Bmal1 and Hnf4α may control susceptibility to liver disease and ultimately, hepatocellular carcinoma. We compared gene expression profiles under conditions of inducible loss of hepatic Hnf4α and inducible loss of Hnf4a and Bmal1 in this RNA-seq experiment. Hepatic Hnf4a (H-KO) or Hnf4a and Bmal1 (BH-KO) were inducibly knocked out after 5 days tamoxifen treatment in eight week-old mice (H-KO) or (BH-KO) followed by vivarium chow or high fat feeding (BH-HF-KO). Littermate control mice (H-WT, BH-WT and BH-HF-WT ) were also treated with tamoxifen at eight weeks of age, but since they lacked the Cre transgene, Hnf4a and Bmal1 expression remained intact. Livers were harvested at 10 weeks of age (BH-WT/KO, H-WT/KO) or 45 weeks ( BH-HF-WT/KO) of age after high fat diet feeding, and liver tissue was flash frozen in liquid nitrogen.

2022-08-01 | GSE173968 | GEO

Microarray of hippocampus from 5mo wt, Bmal1 KO and Nr1d1 (Rev-Erb-alpha) KO mice at a single timepoint

Project description:Deletion of the circadian clock proteins Bmal1 or Nr1d1 (also known as Rev-Erb-alpha) can not only cause circadian dysfunction, but also neuroinflammation in the hippocampus. In this array, 3 wt, 2 Bmal1 KO, and 2 Nr1d1 KO mice, all 5mo, were kept in standard 12h:12h light:dark condition, then anesthetized and perfused with PBS+heparin. Mice were harvest in between noon and 3pm. Whole hippocampus was removed and flash frozen, then RNA was extracted using Trizol reagent and PureLink RNA columns, per manufacturers instructions. RNA microarray analysis was performed by the Washington Univ. Genome Technology Access Center using Agilent Mouse 4x44K mouse V2 array.

2019-02-11 | E-MTAB-7590 | biostudies-arrayexpress

Transcriptome analysis of the circadian clock gene BMAL1 deletion with opposite carcinogenic effects

Project description:We have previously reported that the deletion of BMAL1 gene has opposite effects in respect to its contribution to the pathways that are effective in the multistage carcinogenesis process. BMAL1 deletion sensitized nearly-normal breast epithelial (MCF10A) and invasive breast cancer cells (MDA-MB-231) to cisplatin and doxorubicin-induced apoptosis while this deletion also aggravated the invasive potential of MDA-MB-231 cells. However, the mechanistic relationship of the seemingly opposite contribution of BMAL1 deletion to carcinogenesis process is not known at genome-wide level. In this study, an RNA-seq approach was taken to uncover the differentially expressed genes (DEGs) and pathways after treating BMAL1 knockout (KO) or wild-type (WT) MDA-MB-231 cells with cisplatin and doxorubicin to initiate apoptosis. Gene Set Enrichment Analysis with the DEGs demonstrated enrichment in multiple genes/pathways contribute to sensitization to cisplatin or doxorubicin-induced apoptosis in BMAL1-dependent manner. Additionally, our DEG analysis suggested that non-coding transcripts RNA (such as lncRNA and processed pseudogenes) may have role in cisplatin or doxorubicin-induced apoptosis. Protein-protein interaction network obtained from common DEGs in cisplatin and doxorubicin treatments revealed that GSK3b, NACC1 and EGFR are the principal genes regulating the response of the KO cells. Moreover, the analysis of DEGs among untreated BMAL1 KO and WT cells revealed that epithelial-mesenchymal transition genes are upregulated in KO cells. As a negative control, we have also analyzed the DEGs following treatment with an endoplasmic reticulum (ER) stress-inducing agent, tunicamycin which was affected by BMAL1 deletion minimally. Collectively, the present study suggests BMAL1 regulates many genes/pathways of which the alteration in BMAL1 KO cells may shed light on pleotropic phenotype observed.

2020-08-29 | GSE157069 | GEO

Expression data from peritoneal macrophages stimulated with lipid A

Project description:Setdb1 is one of the H3K9 methyltransferases and represses gene expression by H3K9 methylation. In an attempt to elucidate the role of Setdb1 in the TLR4-mediated inflammatory responses, we performed DNA microarray analysis using lipid A (the active component of LPS)-stimulated peritoneal macrophages from macrophage specific Setdb1 KO (KO) and WT mice. The genes upregulated by lipid A treatment in WT macrophages and further increased in KO macrophages contain many genes associated with interleukins and chemokines. Peritoneal macrophages from WT and KO mice were stimulated with lipid A 10 ng/ml or vehicle for 4 h. Microarray analysis was performed using Affymetrix Mouse 430 2.0.

2016-06-27 | E-GEOD-78153 | biostudies-arrayexpress

Proteomics analysis of regulation by Bmal1 and physiological time-restricted feeding

Project description:To define regulation of tissue proteomes by Bmal1, daily feeding rhythm, and the interaction, we employed Bmal1-stopFL mice, which do not express the main transcriptional activator of the molecular clock, Bmal1, except in cre recombinase-expressing cells1,2 (Figure 1A). Bmal1-stopFL mice lacking cre (Bmal1 knockout, KO) are analogous to Bmal1-null mice and display severely impaired behavioral and molecular rhythms1-3. Hepatocyte-specific Alfp-cre and skeletal muscle-specific Hsa-cre genes were introduced to generate a single line wherein both hepatocyte and skeletal muscle Bmal1 were reconstituted (Liver+Muscle-RE), i.e., rescued (Smith, Koronowski et al. 2023). This approach had the benefit of analyzing liver and muscle from the same mice but comes with the qualification that the abundance of some proteins may be influenced by Bmal1 function in the other tissue, or by a synergistic effect of Bmal1 in both tissues, rather than through rescue of local Bmal1 function alone. Proteomic anlaysis was performed in liver and skeletal muscle.

2024-01-26 | PXD040362 | Pride

The clock gene BMAL1 inhibits macrophage motility, phagocytosis, and impairs defence against pneumonia

Project description:The circadian clock regulates many aspects of immunity. Bacterial infections are affected by time of day, but the mechanisms involved remain undefined. Here we show that loss of the core clock protein BMAL1 in macrophages confers protection against pneumococcal pneumonia. RNAseq was performed on peritoneal macrophages from wild type and BMAL1 knock out mice.

2019-12-20 | E-MTAB-8411 | biostudies-arrayexpress

Expression data from peritoneal macrophages stimulated with lipid A

2016-06-27 | GSE78153 | GEO

WT and aP2-Cre Adipocyte Bmal1 KO 24hr Time Course, Liver Tissue RNA-seq

Project description:Liver metabolism in mice lacking Bmal1 in adipocytes. Comparison between WT and KO revealed no differentially expressed genes at ZT12 and ZT16, and only revealed one gene at ZT8 and ZT20. In contrast many genes were differential at ZT0 and ZT4. With ZT4 having substantially more than ZT0.

2020-06-01 | GSE115264 | GEO

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