Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA330981 | ENA |
REPOSITORIES: ENA
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Project description:Two natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act through the common receptor, guanylyl cyclase-A (GC-A) to lower blood pressure, induce diuresis/natriuresis and dilate blood vessels. Recently, we discovered that the excessive cardiac hypertrophy accompanied with cardiac dysfunction was induced in the lactating natriuretic peptide receptor 1 (Npr1, which encodes GC-A)-deficient mice. To clarify the cause of lactation-induced cardic hypertrophy in Npr1-/-, we performed the gene expressions analysis using nulliparous (NP) or postpartum lactating wild-type (Npr1+/+) and Npr1-/- mice. Numerous genes were altered in the postpartum lactating period both in Npr1+/+ and Npr1-/-. Additionally, the involvement of inflammatory responce in the cardiac hypertrophy in lactating-Npr1-/- mice was clarified bythe gene ontology analysis.
2019-09-01 | GSE84744 | GEO
Project description:Inhibition of fibroblast activation protein promotes cardiac repair by stabilizing brain natriuretic peptide after myocardial infarction
2023-01-26 | GSE184986 | GEO
Project description:Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are not only important biological markers, but also regulators of cardiac functions. The natriuretic peptide A receptor (NPRA), also called NPR1 or guanylyl cyclase A (GC-A), binds with ANP or BNP ligand and fulfils transmembrane signalling transduction by elevating the intracellular levels of cGMP. However, the comprehensive effects and mechanisms downstream to NPRA are still largely to be elucidated. Here, the cardiac expressing profiles of mRNA in the mice with myocardium-specific deletion of NPRA were analyzed. It was found that differently expressed mRNAs were detected and proved by Gene Ontology (GO) and pathway analysis to be mainly related to the metabolic process. Moreover, circular RNAs (circRNAs) were scrutinized, and subsequently a possible regulatory network consisting of circRNAs- MicroRNAs (miRNAs) -mRNAs was predicted and constructed by ceRNA (competing endogenous RNA) analysis. In conclusion, NPRA plays possible roles in cardiac metabolism, which might be mediated by circRNAs via endogenous competition mechanisms.
2020-12-08 | GSE140678 | GEO
Project description:Cardiac hypertrophy is an important and independent risk factor for the development of cardiac myopathy that may lead to heart failure. Cardiac hypertrophy manifests as an enlargement of the individual cardiomyocytes, which impairs the function of the heart. The only way to cure end-stage cardiac myopathy is by heart transplantation, a possibility limited due to lack of donor hearts. Therefore, early diagnosis of cardiac hypertrophy is needed in order to be able to initiate interventions that may prevent further progression of the disease. The mechanisms underlying the development of cardiac hypertrophy are yet not well understood. To increase the knowledge about mechanisms and regulatory pathways involved in the progression of cardiac hypertrophy, we have developed a human induced pluripotent stem cell (hiPSC)-based in vitro model of cardiac hypertrophy and performed extensive characterization of the model using multi-omics analyses. In a series of experiments, hiPSC-derived cardiomyocytes were stimulated with Endothelin-1 for 8, 24, 48 and 72 hours and their transcriptome and secreted proteome were analyzed thoroughly. The transcriptomic data show many enriched canonical pathways related to cardiac hypertrophy already at the earliest time point, e.g., cardiac hypertrophy signaling, actin cytoskeleton signaling and PI3K/AKT signaling. Cluster analysis of the differentially expressed genes showed that there are numerous clusters of genes that are dysregulated over the time period of 8 to 72h. An integrated transcriptome-secretome analysis enabled the identification of multimodal biomarkers of high relevance for monitoring early cardiac hypertrophy progression. Taken together, the results from this study demonstrate that our in vitro model displays a hypertrophic response on transcriptomic- and secreted proteomic level. The results also provide novel insight into the underlying mechanisms of cardiac hypertrophy and novel putative early cardiac hypertrophy biomarkers have been identified that will be further validated to assess their clinical relevance.
2022-02-16 | E-MTAB-11030 | biostudies-arrayexpress
Project description:: The adult heart develops hypertrophy to reduce ventricular wall stress and maintain cardiac function in response to an increased workload. Although pathological hypertrophy generally progresses to heart failure, physiological hypertrophy may be cardioprotective. Cardiac-specific overexpression of the lipid-droplet protein perilipin 5 (Plin5) promotes cardiac hypertrophy, but it is unclear if this response is beneficial. We analyzed human RNA-sequencing data from the left ventricle and showed that cardiac PLIN5 expression correlates with upregulation of cardiac contraction-related processes. To investigate how elevated cardiac Plin5 levels affect cardiac contractility, we generated mice with cardiac-specific overexpression of Plin5 (MHC-Plin5 mice). These mice displayed increased left ventricular mass and cardiomyocyte size but preserved heart function. Quantitative proteomics identified sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) as a Plin5-interacting protein. Phosphorylation of phospholamban, the master regulator of SERCA2, was increased in MHC-Plin5 versus wild-type cardiomyocytes. Live imaging showed increases in intracellular Ca2+ release during contraction, Ca2+ removal during relaxation, and SERCA2 function in MHC-Plin5 versus wild-type cardiomyocytes. These results identify a role for Plin5 in improving cardiac contractility through enhanced Ca2+ signaling.
2023-01-20 | PXD035121 | Pride
Project description:The cardiac natriuretic peptide (NPs) plays an important role in the regulation of cardiovascular and renal function. We examined the miRNAs that could be regulating NPs by subjecting the cardiomyocytes, HCMa cells, to hypoxia.
2015-03-23 | GSE55387 | GEO
Project description:Myocardial hypertrophy develops when the heart is subjected to biomechanical stress, neurohormonal or hemodynamic stimuli. Isoprenaline-induced myocardial hypertrophy in mice exhibited abnormally elevated steroid receptor RNA activator (SRA) level in hypertrophic myocardium, suggesting SRA’s potential functions in hypertrophic pathogenesis. SRA knockout or cardiac-specific knockdown attenuated cardiac remodeling without impairing baseline cardiac function. RNA sequencing and mechanistic studies identified SRA as a transcriptional coactivator that enhances GR-mediated upregulation of HSP70, which in turn activates pro-hypertrophic Akt signaling. Adenoviral SRA overexpression in H9C2 cardiomyocytes amplified isoprenaline-triggered hypertrophic gene expression via this GR-HSP70-Akt axis. Those findings establish SRA as a stress-responsive regulator of maladaptive cardiac growth and propose SRA inhibition as a targeted therapeutic strategy for hypertrophy-related cardiomyopathy. This work bridges noncoding RNA biology with metabolic signaling in heart disease, offering both mechanistic insights and translational potential.
2025-06-30 | GSE300259 | GEO
Project description:Limbs and vertebrae elongate by endochondral ossification, but local growth control is highly modular such that not all bones are the same length. Compared to limbs, which have a different evolutionary and developmental origin, far less is known about how individual vertebrae establish proportion. Using the jerboa and mouse tail skeleton, we find that cell number is a common driver of limb and vertebral proportion in both species. However, chondrocyte hypertrophy, which is a major driver proportion in all mammal limbs, is limited to the extreme disproportionate growth of jerboa mid-tail vertebrae. The genes associated with differential growth in the vertebral skeleton overlap significantly but not substantially with genes associated with limb proportion. Among shared candidates, loss of Natriuretic Peptide Receptor 3 in mice causes disproportionate elongation of the proximal and mid-tail vertebrae, in addition to the proximal limb. Our findings therefore reveal cellular and molecular processes tuning growth of individual vertebrae while also identifying natriuretic peptide signaling among genetic control mechanisms that shape the entire skeleton.
2025-06-15 | GSE299515 | GEO
Project description:A balanced activity of cGMP signaling contributes to the maintenance of cardiovascular homeostasis. Vascular smooth muscle cells (VSMCs) can generate cGMP via three ligand-activated guanylyl cyclases, the NO-sensitive guanylyl cyclase, the atrial natriuretic peptide (ANP)-activated GC-A, and the C-type natriuretic peptide (CNP)-stimulated GC‑B. Here, we studied natriuretic peptide signaling in murine VSMCs and atherosclerotic lesions. Correlative profiling of pathway activity and VSMC phenotype at the single-cell level showed that phenotypic modulation of contractile VSMCs to chondrocyte-like plaque cells during atherogenesis is associated with a switch from ANP/GC‑A to CNP/GC‑B signaling. Silencing of the CNP/GC-B axis in VSMCs resulted in an increase of chondrocyte-like plaque cells. These findings indicate that the CNP/GC‑B/cGMP pathway is a marker and atheroprotective regulator of modulated VSMCs, limiting their transition to chondrocyte-like cells. Overall, this study highlights the plasticity of cGMP signaling in VSMCs and suggests analogies between CNP-dependent remodeling of bone and blood vessels.
2024-12-17 | GSE282944 | GEO
Project description:Cardiac hypertrophy consists in the enlargement of cardiomyocytes and alteration of the extracellular matrix organization in response to physiological or pathological stress. In pathological hypertrophy ocuurs myocardial damage, loss of cardiomyocytes, fibrosis, inflammation, sarcomere disorganization and metabolic impairment, leading to cardiac dysfunction.The rodent model treated with isoproterenol induces cardiac hypertrophy due the constant activation of β-adrenergic receptors. We conducted a quantitative label-free proteomic analysis of cardiomyocytes isolated from hearts of mice treated or not with isoproterenol to better understand the molecular bases of cellular response due to isoproterenol-induced injury.
2020-05-27 | PXD013020 | Pride