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Effect of conditional deletion of Bmal1 in pancreatic β-cells in modulating transcriptional islet response to STZ-mediated pro-inflammatory injury

ABSTRACT: Effect of conditional deletion of Bmal1 in pancreatic β-cells in modulating transcriptional islet response to STZ-mediated pro-inflammatory injury

PROVIDER: PRJNA1168494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30872960_1.fastq.gz	Fastqsanger.gz
	SRR30872960_2.fastq.gz	Fastqsanger.gz
	SRR30872961_1.fastq.gz	Fastqsanger.gz
	SRR30872961_2.fastq.gz	Fastqsanger.gz
	SRR30872962_1.fastq.gz	Fastqsanger.gz

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Effect of conditional deletion of Bmal1 in pancreatic β-cells in modulating transcriptional islet response to STZ-mediated pro-inflammatory injury

Project description:The circadian clock plays a vital role in modulating the cellular immune response. However, its role in mediating pro-inflammatory diabetogenic β-cell injury remains largely unexplored. Our studies demonstrate that conditional deletion of Bmal1 in mouse β-cells was shown to impair the ability of β-cells to recover from streptozotocin-mediated pro-inflammatory injury in vivo, leading to β-cell failure and the development of diabetes. Our study suggests that the β-cell circadian clock mediates β-cell response and recovery from pro-inflammatory injury common to the pathogenesis of diabetes mellitus.

2024-10-31 | GSE278711 | GEO

Gene expression profile at single cell level of GFP labeled islet β cells from streptozotocin (STZ) treated Ins/β-lineage-labeled mice

Project description:Islet β cells suffer from de- and trans-differentiation after injury. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of β cells in from STZ-induced diabetes.

2023-05-01 | GSE203042 | GEO

RNA-seq of islet, FACS- sorted CD45+Ly6C-CD11B+CD11C+F4/80+ cells from C57bl6/J male mice that were treated with low dose streptozotocin (STZ) or acetate buffer

Project description:The experiment was designed to obtain a broader unbiased view of the changes in islet macrophages following low dose STZ challenge. Mice were purchased from Jackson Laboratory (Bar Harbor, ME). 16-20-week-old C57BL/6J males were given 30 mg/kg STZ or acetate buffer (control) i.p. (intraperitoneal injection) for 5 consecutive days. Following the first STZ or buffer injection mice were sacrificed on day 14 and islets were isolated by collagenase digestion. Freshly isolated islets were dispersed in 0.02% Trypsin-EDTA for 3 minutes followed by up to 1 minute of pipetting under a stereomicroscope to obtain a single cell solution. Islet media was added to stop the reaction. Islets from 10 mice were pooled per sample (N). Dispersed islets were washed with FACS buffer (1% heat inactivated FBS, 1 mM EDTA, 11 mM glucose in PBS). Cells were kept on ice and pre-incubated with Fc Block (1:100) for 5 minutes, followed by 30 min incubation with CD45-eFluor 450 (1:250; clone 30-F11), Ly-6C-APC (1:1,200; clone HK1.4), CD11b-PE (1:1,200; clone M1/700, F4/80-FITC (1:150; clone BM8), CD11c-PECy7 (1:150; clone N418), and the viability dye 7AAD (1:2,000). Unstained, single stains, and fluorescence minus one controls were used for setting gates and compensation. Viable, single CD45+Ly6c-Cd11b+Cd11c+F4/80+ cells were sorted using a BD FACS Aria IIu directly into lysis buffer, and the RNeasy Plus Micro Kit from Qiagen was used to isolate total RNA. Total RNA quality control quantification was performed using an Agilent 2100 Bioanalyzer. All RNA samples had an RNA integrity number (RIN) ≥9.1. The NeoPrep Library Prep System from Ilumina was used for library preparation followed by sequencing using standard Illumina methods and Ilumina NextSeq500.

2019-11-01 | E-MTAB-7234 | biostudies-arrayexpress

The BMAL1/HIF2A heterodimer modulates circadian variations of myocardial injury

Project description:Cardiac injury following myocardial infarction exhibits a circadian pattern, yet the underlying mechanism remains unclear. To elucidate genes governing circadian variation of myocardial injury, we conducted transcriptomic profiling of left-ventricular tissues from mice or humans experiencing myocardial injury at different daytimes. Through comprehensive analyses, including transgenic mouse models and functional studies, we identified BMAL1 as a pivotal transcription factor modulating diurnal variation of myocardial injury. Remarkably, we discovered that BMAL1 regulates circadian-dependent cardiac injury by forming a transcriptionally active heterodimer with HIF2A. Substantiating this finding, we determined the cryo-EM structure of the BMAL1/HIF2F/DNA complex, revealing a previously unknown capacity for structural rearrangement within BMAL1. Furthermore, we confirmed amphiregulin (AREG) as a transcriptional target of the BMAL1/HIF2A heterodimer, critical for modulating circadian variation of myocardial injury. Finally, targeting the BMAL1/HIF2A-AREG pathway via timed AREG administration or enhancing circadian rhythm pharmacologically offered significant cardioprotection, implicating this pathway in treating ischemic heart disease.

2024-03-20 | GSE255307 | GEO

Transcriptional characterization of intestinal ILC3 lacking BMAL1

Project description:Small intestinal group 3 innate lymphoid cells (ILC3) from ILC3-conditional BMAL1 knock out mice or littermate control mice were sort-purified for transcriptional analysis

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Liraglutide effect on STZ Mouse Kidney with diabetic nephropathy

Project description:The effect of liraglutide on the kidney proteome in the STZ mouse model compared to healthy and STZ diabetic control groups.

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Transcriptional Repressor Gm129 Modulates the Circadian Gene Expression by Inhibiting CLOCK:BMAL1 Activity

Project description:The mammalian circadian clock is a molecular oscillator composed of a feedback loop that involves transcriptional activators CLOCK and BMAL1, and repressors Cryptochrome (CRY) and Period (PER). Here we show that a direct CLOCK-BMAL1 target gene, Gm129, is a novel regulator of the feedback loop. ChIP analysis revealed that the CLOCK:BMAL1:CRY1 complex strongly occupies the promoter region of Gm129. Both mRNA and protein levels of GM129 exhibit high amplitude circadian oscillations in mouse liver, and Gm129 gene encodes a nuclear-localized protein that directly interacts with BMAL1 and represses CLOCK:BMAL1 activity. In vitro and in vivo protein-DNA interaction results demonstrate that, like CRY1, GM129 functions as a repressor by binding to the CLOCK:BMAL1 complex on DNA. Although Gm129-/- or Cry1-/- Gm129-/- mice retain a robust circadian rhythm, the peaks of Nr1d1 and Dbp mRNAs in liver exhibit significant phase delay compared to control. Our results suggest that, in addition to CRYs and PERs, GM129 protein contributes to the transcriptional feedback loop by modulating CLOCK:BMAL1 activity as a transcriptional repressor. Examination of 3 transcriptional regulators in mouse liver

2014-01-07 | E-GEOD-53828 | biostudies-arrayexpress

TMT analysis of proteomic changes in the gastrocnemius skeletal muscles of WT and Bmal1-KO mice, and Bmal1-KO mice rescued with AAV-mediated muscle-specific expression of Bmal1.

Project description:TMT analysis of proteomic changes in the gastrocnemius skeletal muscles of WT and Bmal1-KO mice, and Bmal1-KO mice rescued with AAV-mediated muscle-specific expression of Bmal1.

2024-10-03 | PXD054406 | Pride

Ghrelin deletion and conditional ghrelin-cell ablation increase pancreatic islet size in mice

Project description:Ghrelin deletion and conditional ghrelin-cell ablation increase pancreatic islet size in mice

| PRJNA1022509 | ENA

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

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