Project description:Diabetes mellitus (DM) causes the change in the components of the plasma, which may induce tissue and organ injuries, including the heart and kidney. In the diabetic model db/db mice, intravenous injection of purified dipeptidyl peptidase III (DPPIII) attenuated the heart and kidney damages provoked by DM without alteration in blood glucose level. This led us to hypothesize that there might be peptide(s) that are involved in the progression of the DM-mediated damages and are cleaved by DPPIII. To explore the peptides, the whole peptidomics analysis was conducted using tandem mass spectrometry, in which peptides derived from the plasma of PBS-infused C57BL/6 mice, PBS-infused db/db mice, and DPPIII-treated db/db mice were compared. All of the lists of the peptides in the three mouse groups were shown in the raw data formatted and excel files.
Project description:Diabetes mellitus (DM) causes the change in the components of the plasma, which may induce tissue and organ injuries, including the heart and kidney. In the diabetic model db/db mice, intravenous injection of purified dipeptidyl peptidase III (DPPIII) attenuated the heart and kidney damages provoked by DM without alteration in blood glucose level. This led us to hypothesize that there might be peptide(s) that are involved in the progression of the DM-mediated damages and are cleaved by DPPIII. To explore the peptides, the whole peptidomics analysis (shotgun peptidomics) was conducted using tandem mass spectrometry, in which peptides derived from the plasma of PBS-infused C57BL/6 mice, PBS-infused db/db mice, and DPPIII-treated db/db mice were compared. The raw mass spectrometry data were deposited to the ProteomeXchange with the dataset identifier PXD025440. Together with the mass spectrometry analysis and other experiments, we identified a peptide named Peptide 2 (AA sequence: RLLWENGNL) as a substrate of DPPIII. Peptide 2 is a part of C3f (53% identical), and C3f can act as an anaphylatoxin like C3a. To quantify the amount in plasma derived from the plasma of PBS-infused C57BL/6 mice, PBS-infused db/db mice, and DPPIII-treated db/db mice, selected reaction monitoring (SRM) assay was performed. All of the chromatograms and quantified data obtained by SRM from the three mouse groups were shown in the Analyst formated and PDF files.
Project description:To identify putative lncRNA changes in the livers of db/db mice and C57 mice, we isolated the liver tissues and carried out a microarray analysis. Here, we found significant changes of lncRNAs in the livers of db/db mice. Among them, abnormal expression of ultraconserved elements was noticed.
Project description:Analysis of single cell RNA-seq, CITE-seq data and bulk RNA-seq data on cells isolated from the livers of mice following PBS and APAP (paracetamol/acetaminophen) administration. Spatial Transcriptomics analysis was performed using 10x Visium platform on mouse livers 48hrs post PBS or APAP administration. We also analysed single cell RNA-seq data on CD64+F4/80+ macrophages isolated from the livers of Trem2 fl/fl mice and CD64CRE Trem2 fl/fl mice.
Project description:Analysis of single cell RNA-seq, CITE-seq data and bulk RNA-seq data on cells isolated from the livers of mice following PBS and APAP (paracetamol/acetaminophen) administration. Spatial Transcriptomics analysis was performed using 10x Visium platform on mouse livers 48hrs post PBS or APAP administration. We also analysed single cell RNA-seq data on CD64+F4/80+ macrophages isolated from the livers of Trem2 fl/fl mice and CD64CRE Trem2 fl/fl mice.
Project description:Analysis of single cell RNA-seq, CITE-seq data and bulk RNA-seq data on cells isolated from the livers of mice following PBS and APAP (paracetamol/acetaminophen) administration. Spatial Transcriptomics analysis was performed using 10x Visium platform on mouse livers 48hrs post PBS or APAP administration. We also analysed single cell RNA-seq data on CD64+F4/80+ macrophages isolated from the livers of Trem2 fl/fl mice and CD64CRE Trem2 fl/fl mice.
Project description:In metabolic control, GC signaling acts as a major counter-regulatory system against insulin action, and aberrantly elevated GC activity is tightly linked to major components of the so-called Metabolic Syndrome, including obesity, insulin resistance, hyperglycemia, and systemic dyslipidemia. Here we identify the hepatic induction of the conserved microRNA (miR)-379/410 genomic cluster as a key component of GC/GR-driven metabolic dysfunction in M-bM-^@M-^\diabesityM-bM-^@M-^] Microarray data were utilized to screened for differentially regulated miRNAs between wt and db/db and between wt and GR Knockdown mice For wt vs. db/db: mice were fasted for 24 hours and refed for 6 hours; For GR-dependent miRNAs: mice were treated with rAAV delivering either control or GR-directed miRNA for the knockdown of the GR specifically in the liver.
Project description:We compared proteinase K buffer (PKBuffer) vs TRIzol vs column-based (PureLink RNA Micro kit) RNA isolation on frozen mouse organs methods using the high throughput CryoGrid system integrated with PIXUL sonicator. Mice were treated with intraperiteal injection of LPS (model of endotoxin induced sepsis) or PBS (control). After 12 hours mice were euthanized and brains, hearts, kidneys, and livers were harvested, immediately placed on ice, and then frozen in CryoTrays.
Project description:Purpose: RNAseq analyses were conducted to screen for the genes undergoing transcriptional changes either in the liver of high-fat-diet (HFD)-induced obese mice or in the liver of Lepr-deficient db/db mice compared to the livers of the respective control mice Methods: C57BL/6 wild-type male mice were fed on high-fat diet (HFD) or a low-fat diet (NCD) for 18 weeks starting from 6 weeks of age, and the livers were collected at 24 weeks of age at ad libitum-fed condition.Misty/misty or db/db were sacrificed at ad libitum-fed condition at 10weeks and the liver was collected. Results: 2079 genes and 1085 genes were identified in high-fat-diet fed mice and db/db mice, respectively.
