Transcriptome of cardiac tissue from WT mice, cardiac macrophages depleted mice, and mice deficient for Mertk and LxR
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE106295 | GEO | 2018/10/27
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptome of cardiac tissue from WT mice, cardiac macrophages depleted mice, and mice deficient for Mertk and LxR
| PRJNA416139 | ENA
Project description:The mammalian circadian timing system coordinates key molecular, cellular and physiological processes along the 24-h cycle. Accumulating evidence suggests that many clock-controlled processes display a sexual dimorphism. In mammals this is well exemplified by the difference between the male and female circadian patterns of glucocorticoid hormone secretion and clock gene expression. Here we show that the non-circadian nuclear receptor and metabolic sensor Liver X Receptor alpha (LXR?) which is known to regulate glucocorticoid production in mice modulates the sex specific circadian pattern of plasma corticosterone. Lxr?(-/-) males display a blunted corticosterone profile while females show higher amplitude as compared to wild type animals. Wild type males are significantly slower than females to resynchronize their locomotor activity rhythm after an 8 h phase advance but this difference is abrogated in Lxr?(-/-) males which display a female-like phenotype. We also show that circadian expression patterns of liver 11?-hydroxysteroid dehydrogenase type 1 (11?-HSD1) and Phosphoenolpyruvate carboxykinase (Pepck) differ between sexes and are differentially altered in Lxr?(-/-) animals. These changes are associated with a damped profile of plasma glucose oscillation in males but not in females. Sex specific alteration of the insulin and leptin circadian profiles were observed in Lx?(-/-) females and could be explained by the change in corticosterone profile. Together this data indicates that LXR? is a determinant of sexually dimorphic circadian patterns of key physiological parameters. The discovery of this unanticipated role for LXR? in circadian physiology underscores the importance of addressing sex differences in chronobiology studies and future LXR? targeted therapies.
| S-EPMC4777295 | biostudies-literature
Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs cardiomyocyte regeneration or promotes maladaptive remodeling, leading to compromised cardiac function.
2024-12-02 | E-MTAB-14508 | biostudies-arrayexpress
Project description:Supplement of high-protein food plays an important role in improving the symptoms of malnutrition and the immune capacity of the body, but the association of high-protein diet and gut microbiota remained unaddressed. Here, we systematically analyzed the internal organs and gut microbiota in C57(WT) or PD-1H-depleted (KO) mice (T cells were activated) fed with pupae or feed for six weeks. We observed that the body weight gain in the mice fed with pupae increased less significantly than that of the feed group, while the villi and small intestine lengths in the pupa group were reduced compared with that of mice given feed. However, the average body weight of the KO mice increased compared with that of the WT mice fed with pupae or feed. Pupae increased the concentration of blood glucose in WT, but not in KO mice. Moreover, in the feed group, there was no difference in the weight of the internal organs between the WT and KO mice, but in the pupae-fed group, liver weight was decreased and spleen weight was increased compared with that of KO mice. The amounts/plural/amounts of Melainabacteria, Chloroflexi, and Armatimonadetes were specifically upregulated by pupae, and this upregulation was weakened or eliminated by PD-1H depletion. Some bacteria with high abundance in the feed-fed KO mice, such as Deferribacteres, Melainabacteria, Acidobacteria, Bacteroidetes, Spirochaetes and Verrucomicrobia, were decreased in pupae-fed KO mice, and Proteobacteria and Deinococcus were specifically enriched in pupae-fed KO mice. Bacteroidetes, Firmicutes and Akkermansia were associated with weight loss in the pupaefed group while Lachnospiraceae and Anaerobiospirillum were related glucose metabolism and energy consumption. Based on high-throughput sequencing, we discovered that some gut bacteria specifically regulated the metabolism of a high-protein diet, and PD-1H deficiency improved life quality and sustained blood glucose. Moreover, PD-1H responses to high-protein diet through modulating the type and quantity of gut bacteria. These findings provide evidence about the association among gut microbiota, T cell activation (for PD-1H depletion) and high-protein diet metabolism, have important theoretical significance for nutrition and health research.
| S-EPMC9705843 | biostudies-literature
Project description:To determine if the absence of FKBP12 in cardiac tissue alters JPH2 interactions with other dyadic proteins, we immunoprecipitated JPH2 from hearts of FL, MCK-FKD, MHC-Cre+ only, and MHC-FKD mice. Specific proteins were identified in the IPs from the FL mice and included JPH2, CASQ2 , SPEG, RYR2, CACNA1c, CACNB2, ESD, CMYA5, and LRRC10.
2024-03-19 | MSV000094363 | MassIVE
Project description:Dysferlin is expressed in skeletal and cardiac muscle. However, dysferlin deficiency, namely limb girdle muscular dystrophy 2B (LGMD2B) and Myoshi myopathy, results in skeletal muscle weakness and spares the heart. This dichotomy could be caused by differential regulation of protective mechanisms. Therefore, we compared intraindividual mRNA expression profiles between cardiac and skeletal muscle in dysferlin-deficient SJL/J mice and normal C57BL/6 mice. Keywords: parallel sample
2005-07-10 | GSE2507 | GEO
Project description:To investigate the altered methylation cardiac-specific NPRA-deficient mice compares to wild type, methylation level alterations were detected by Arraystar Mouse m6A Single Nucleotide resolution microarray analysis (mazF-RIP) using the myocardium from NPRA-deficient (NPRA-/-) mice and wild-type (NPRA+/+) mice as control.
2022-07-01 | GSE181039 | GEO
Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte (CM) proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.
2024-10-31 | E-MTAB-14505 | biostudies-arrayexpress
Project description:Purpose:Atypical classical chemokine receptor 4 (ACKR4) is a newly reported atypical classical chemokine receptor. However, its expression and role in MI are still unknown. This study aims to determine whether ACKR4 modulates cardiac remodeling following MI and to explore the specific molecular mechanism. Methods: RNA sequencing of infarcted hearts from WT and ACKR4-KO mice was performed at day 14 post-MI. Results: We generated a library of distinct transcriptome expression patterns.The consistency in the clustering suggested a homogeneous genomic activity with limited background signal and high levels of reproducibility across the three biological replicates in each group.Utilizing a P value < 0.05 and fold changes of 1.5 or greater, we identified 774 genes that are differentially expressed in ACKR4-KO mice compared to WT mice.The downregulated-genes belonged to the GO classes taxis, chemotaxis, extracellular matrix, and cytokine activity. Conclusions: These data provide the first insight into the role and mechanism of ACKR4 in MI.
2021-02-24 | GSE161415 | GEO
Project description:Dysferlin is expressed in skeletal and cardiac muscle. However, dysferlin deficiency, namely limb girdle muscular dystrophy 2B (LGMD2B) and Myoshi myopathy, results in skeletal muscle weakness and spares the heart. This dichotomy could be caused by differential regulation of protective mechanisms. Therefore, we compared intraindividual mRNA expression profiles between cardiac and skeletal muscle in dysferlin-deficient SJL/J mice and normal C57BL/6 mice. Experiment Overall Design: 20 chips were analyzed. They represent 4 groups of 5 replicates each. Experiment Overall Design: The 4 groups are cardiac (LV) and skeletal muscle of normal and dysferlin deficient mice. Experiment Overall Design: Tissues from normal mice are the controls in comparison to tissues of dysferlin deficient mice.
2007-09-04 | E-GEOD-2507 | biostudies-arrayexpress