Project description:Mice without cardiac Bmal1 function develop severe progressive heart failure with age. To examine the mechanism underlying the failing heart phenotype observed in heart-specific Bmal1 knockout mice, microarray analyses were performed. The analyses revealed that broad classes of genes regulating cellular energy metabolism were upregulated or downregulated in the heart tissues of heart-specific Bmal1 knockout mice compared with those of control animals. Heart total RNA extracted from six animals per genotype (control and heart-specific Bmal1 knockout) was pooled and then used for a microarray analysis.
Project description:Mice without cardiac Bmal1 function develop severe progressive heart failure with age. To examine the mechanism underlying the failing heart phenotype observed in heart-specific Bmal1 knockout mice, microarray analyses were performed. The analyses revealed that broad classes of genes regulating cellular energy metabolism were upregulated or downregulated in the heart tissues of heart-specific Bmal1 knockout mice compared with those of control animals.
Project description:Subcutanesouly tumors from both Bmal1+/+ and Bmal1-/- mice were used to isolated stromal vascular fractions (SVF). Tumor cells with GFP+ signals were exclusive. Remain GFP- cells were collected to do RNAseq.
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
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.
Project description:This is an investigation of whole genome gene expression level in tissues of mice stimulated by LPS, FK565 or LPS + FK565 in vivo and ex vivo. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in aortic root including aortic valves, slight in aorta and absent in other arteries. The degree of respective vascular inflammation is associated with persistent high expression of proinflammatory chemokine/cytokine genes in each tissue in vivo by microarray analysis, and not with Nod1 expression levels. The ex vivo production of proinflammatory chemokine/cytokine by Nod1 ligand is higher in aortic root than in other arteries from normal murine vascular tissues, and also higher in human coronary artery endothelial cells (HCAEC) than in human pulmonary artery endothelial cells (HPAEC), suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular tissue/cell itself.
