Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of depletion of vacuolar protein sorting 13 homolog c (Vps13c) in heart tissue from ventricles of wild-type (WT) and cardiac-specific knockout (Vps13c-cKO) mice.

ABSTRACT: Systems genetics strategy across multiple Hybrid Mouse Diversity Panel (HMDP) cohorts pinpointed vacuolar protein sorting 13 homolog c (Vps13c) as a candidate trans-regulator of the mitochondrial transcriptome. Subsequent functional studies revealed that VPS13C influences mitochondrial morphology, bioenergetics, and global gene expression in cardiomyocytes. To assess the in vivo role of Vps13c, we generated Vps13c-flox mice, which were further crossed with Myh6-Cre mice to generate cardiac-specific knockout (Vps13c-cKO) mice. Efficient gene deletion was confirmed by reduced cardiac Vps13c mRNA and protein levels. RNA sequencing of ventricles from WT and Vps13c-cKO mice were performed here to investigate the impact of loss of Vps13c in vivo.

ORGANISM(S): Mus musculus

PROVIDER: GSE307260 | GEO | 2025/09/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Role of SPOP in cardiac hypertrophy and heart failure

Project description:Pressure overload-induced cardiac hypertrophy and heart failure involve profound remodeling of the myocardial proteome. To elucidate the role of the E3 adaptor protein SPOP in this process, we performed TMT-based quantitative proteomic analysis on left ventricular tissues collected four weeks after transverse aortic constriction (TAC) from Myh6-Cre control mice (n=5) and cardiac-specific SPOP knockout (cKO) mice (n=5).

2025-08-26 | PXD067120 | Pride

Effect of depletion of vacuolar protein sorting 13 homolog c (Vps13c) in heart tissue from ventricles of wild-type (WT) and cardiac-specific knockout (Vps13c-cKO) mice.

Project description:Effect of depletion of vacuolar protein sorting 13 homolog c (Vps13c) in heart tissue from ventricles of wild-type (WT) and cardiac-specific knockout (Vps13c-cKO) mice.

| PRJNA1315041 | ENA

Transcriptome profiling of left ventricles from cardiac-specific miR-150 conditional knockout mice

Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from cardiac-specific miR-150 conditional knockout KO (cKO) mice were performed to identify novel miR-150 targets in the heart.

2021-08-18 | GSE177057 | GEO

MED13cTg heart ventricles and epididymal fat

Project description:The heart requires a continuous supply of energy but has little capacity for energy storage and thus relies on exogenous metabolic sources. We previously showed that cardiac MED13 modulates systemic energy homeostasis in mice. Here we sought to define the extra-cardiac tissue(s) that respond to cardiac MED13 signaling. We show that cardiac over-expression of MED13 in transgenic (MED13cTg) mice confers a lean phenotype that is associated with increased lipid uptake, beta-oxidation and mitochondrial content in white adipose tissue (WAT) and liver. Cardiac expression of MED13 decreases metabolic gene expression and metabolite levels in heart and liver but enhances them in WAT. Although exhibiting increased energy expenditure in the fed state, MED13cTg mice metabolically adapt to fasting. Furthermore, MED13cTg hearts oxidize fuel that is readily available, rendering them more efficient in the fed state. Parabiosis experiments in which circulations of wild-type and MED13cTg mice are joined, reveal that circulating factor(s) in MED13cTg mice promote enhanced metabolism and leanness. These findings demonstrate that MED13 acts within the heart to promote systemic energy expenditure in extra-cardiac energy depots and point to an unexplored metabolic communication system between the heart and other tissues.

2014-12-01 | GSE62450 | GEO

Klf9 is essential for cardiac mitochondrial homeostasis

Project description:Mitochondrial dynamics and mitophagy are intimately linked physiological processes that are essential for cardiac homeostasis. Here we show that cardiac Klf9 is dysregulated in human and rodent cardiomyopathy. Young adult global Klf9-knockout mice displayed hypertrophic cardiomyopathy that was characterized by depressed systolic function, increased left ventricular mass and pulmonary congestion. Klf9 knockout led to mitochondrial disarray and fragmentation in cardiomyocytes. Biochemical analysis confirmed that mitochondrial respiratory function was impaired in Klf9-knockout cardiomyocytes, with reduced myocardial ATP levels and elevated ROS. Furthermore, cardiac-specific Klf9-deficient mice phenocopied global Klf9-knockout mice, suggesting that cardiac Klf9 is essential for mitochondrial homeostasis and heart function. Moreover, cardiac Klf9 deficiency inhibited mitophagy induced by angiotensin II (ANGII), thereby leading to accumulation of dysfunctional mitochondria and acceleration of heart failure in mice in response to ANGII treatment. In contrast, cardiac-specific Klf9 transgene improved cardiac systolic function via promoting mitophagy in mice in response to ANGII treatment. Molecular mechanism studies indicated that Klf9 knockout decreased the expression of PGC-1α and its target genes involved in mitochondrial energy metabolism. Moreover, Klf9 controlled the expression of Mfn2 by directly binding to its promoter region, thereby regulating mitochondrial dynamics and mitophagy. Finally, we performed Mfn2 rescue experiments in Klf9-CKO mice and found that AAV-mediated Mfn2 rescue in heart improved cardiac mitochondrial and systolic function in Klf9-CKO mice treated with or without ANGII. Thus, Klf9 integrates cardiac energy metabolism, mitochondrial dynamics and mitophagy. Modulating Klf9 activity may have therapeutic potential in the treatment of heart failure.

2024-10-03 | GSE278326 | GEO

RNA-seq comparing the WT mouse hearts versus Dhx36 cKO hearts

Project description:This experiment aimed to investigate the transcriptional role of G4 resolvase Dhx36 in the adult mouse heart. We compared three pools of wild-type (WT) mouse hearts with three pools of Dhx36 conditional knockout (cKO) hearts. In the mutant mice, Dhx36 was conditionally deleted in cardiomyocytes using the Myh6-cre transgenic line. Each of the six pools was created using RNA extracted from 3-5 hearts from mice aged approximately 21 days. The cKO mice developed dilated cardiomyopathy and began experiencing sudden death at 40 days old, with no mutants surviving beyond 5 months.

2024-09-15 | E-MTAB-14440 | biostudies-arrayexpress

RNA-Seq for control and Znhit1-deficient heart tissues from postnatal day 17 and 25 mice

Project description:To investigate the function of Znhit1 in mouse hearts, we deleted Znhit1 using conditional Znhit1-knockout mice (Znhit1 flox/flox; Myh6-Cre; Znhit1 cKO). Through RNA-Seq, we tested the genome-wide transcriptional changes at postnatal day 17 and 25.

2022-04-19 | GSE194115 | GEO

Proteomic analysis of the cardiac muscle from the HMDP

Project description:Mitochondria play a key role in the normal function of the heart as well as in the pathogenesis of diseases. We report analysis of common genetic variations contributing to mitochondrial and heart functions using an integrative proteomics approach in a panel of inbred mouse strains called the Hybrid Mouse Diversity Panel (HMDP). We performed a whole heart proteomic analysis in the HMDP (72 strains, n=2-3 mice) and retrieved 840 mitochondrial proteins (quantified in ≥50 strains).

2023-06-01 | PXD036398 | Pride

Cardiomyocyte-specific Srsf3 deletion reveals a mitochondrial regulatory role

Project description:Serine-rich splicing factor 3 (SRSF3) was recently reported as being necessary to preserve RNA stability via an mTOR mechanism in a cardiac mouse model in adulthood. Here, we demonstrate the link between Srsf3 and mitochondrial integrity in an embryonic cardiomyocyte-specific Srsf3 conditional knockout (cKO) mouse model. Fifteen-day-old Srsf3 cKO mice showed dramatically reduced (below 50%) survival and reduced the left ventricular systolic performance, and histological analysis of these hearts revealed a significant increase in cardiomyocyte size, confirming the severe remodeling induced by Srsf3 deletion. RNA-seq analysis of the hearts of 5-day-old Srsf3 cKO mice revealed early changes in expression levels and alternative splicing of several transcripts related to mitochondrial integrity and oxidative phosphorylation. Likewise, the levels of several protein complexes of the electron transport chain decreased, and mitochondrial complex I-driven respiration of permeabilized cardiac muscle fibers from the left ventricle was impaired. Furthermore, transmission electron microscopy analysis showed disordered mitochondrial length and cristae structure. Together with its indispensable role in the physiological maintenance of mouse hearts, these results highlight the previously unrecognized function of Srsf3 in regulating the mitochondrial integrity.

2021-06-23 | GSE151168 | GEO

Tumor Necrosis Factor Associated Factor 2 Mediates Cardiac Protection Through Non-canonical NF-κB Signaling

Project description:To elucidate the mechanisms responsible for cytoprotective effects of tumor necrosis factor receptor activated factor 2 (TRAF2) in the heart, we employed genetic gain and loss of function studies ex vivo and in vivo in mice with cardiac restricted overexpression of TRAF2 (Myh6-TRAF2LC). Crossing Myh6-TRAF2LC mice with mice lacking canonical signaling (Myh6-TRAF2LC/Myh6-IκBαΔN) abrogated the cytoprotective effects of TRAF2 ex vivo. In contrast, inhibiting the JAK/STAT pathway did not abrogate the cytoprotective effects of TRAF2. Transcriptional profiling of wild-type, Myh6-TRAF2LC, Myh6-TRAF2LC/Myh6-IκBαΔN hearts suggested that the non-canonical NF-κB signaling pathway was upregulated in the Myh6-TRAF2LC hearts. Western blotting and ELISA for the NF-κB family proteins p50, p65, p52 and RelB on nuclear and cytoplasmic extracts from naïve 12 week old wild-type, Myh6-TRAF2LC and Myh6-TRAF2LC/Myh6-IκBαΔN mouse hearts showed increased expression levels and increased DNA binding of p52 and RelB, which are NF-κB family members, whereas there was no increase in expression nor DNA binding of the p50 and p65 subunits. Crossing Myh6-TRAF2LCmice with RelB-/+mice (Myh6-TRAF2LC/RelB-/+) attenuated the cytoprotective effects of TRAF2 ex vivo and in vivo. Viewed together, these results suggest that cross-talk between the canonical and non-canonical NF-κB signaling pathways is required for mediating the cytoprotective effects of TRAF2.

2017-12-15 | GSE107668 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data