Pulmonary artery banded rat heart
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Rattus Norvegicus (rat)
TISSUE(S): Heart
SUBMITTER: 
Josh Maxwell
LAB HEAD: Josh Maxwell
PROVIDER: PXD027427 | Pride | 2022-05-20
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Deamidation__NQ_Sites.txt | Txt | |||
| Oxidation__M_Sites.txt | Txt | |||
| Phospho__STY_Sites.txt | Txt | |||
| allPeptides.txt | Txt | |||
| evidence.txt | Txt |
Items per page: 5 1 - 5 of 33 |
Publications
Loss of cardiac myosin light chain kinase contributes to contractile dysfunction in right ventricular pressure overload.
Prasad Vidhya V Makkaoui Nour N Rajan Rohan R Patel Alisha A Mainali Bipul B Bagchi Pritha P Kumar Rhea R Rogers Julia J Diamond Jake J Maxwell Joshua T JT
Physiological reports 20220401 7
Nearly 1 in every 100 children born have a congenital heart defect. Many of these defects primarily affect the right heart causing pressure overload of the right ventricle (RV). The RV maintains function by adapting to the increased pressure; however, many of these adaptations eventually lead to RV hypertrophy and failure. In this study, we aim to identify the cellular and molecular mechanisms of these adaptions. We utilized a surgical animal model of pulmonary artery banding (PAB) in juvenile r ...[more]
Similar Datasets
Project description:We utilized an animal model of RV pressure overload created by banding the pulmonary artery (PAB). Two weeks post-banding, bone marrow-derived mesenchymal stromal cells (MSCs) and 3 populations of CPCs (nCPCs, cCPCs, ES-CPCs) were delivered to the RV free wall. RV function and cellular retention were measured for four weeks post-injection, at which point hearts were extracted and the RV was excised for liquid chromatography and tandem mass spectrometry. Resulting RV proteomes were compared and analyzed using systems biology and bioinformatics.
2024-10-17 | PXD051582 | Pride
Project description:We exploit the predictable time course of Drosophila brain development to perform a temporally coupled quantitative proteomic analysis of the pupal brain in Nab2 mutant or overexpression models, which reveals that Nab2 is required to regulate the abundance of a number of proteins with critical roles in Drosophila neurons. Pupal brains lacking Nab2 show dysregulation of proteins, such as Futsch, Turtle, Contactin, and Van Gogh, that typically function in brain morphogenesis, neuroblast proliferation, circadian sleep/wake cycle, and other neurodevelopmental processes. Overall, these data define a role for Nab2 during neurodevelopment in regulating protein abundance for a subset of the brain proteome and provide a window into the potential functions of human ZC3H14 protein.
2022-02-17 | PXD022984 | Pride
Project description:Fragile X syndrome (FXS), the most common inherited intellectual disability and monogenic cause of autism, results from loss of FMRP, which regulates mRNA translation essential for brain development and synaptic plasticity. FMRP has been implicated in the synaptic localization and surface expression of various membrane proteins, yet underlying mechanisms remain unclear. Here, we identified a broad dysregulation of membrane surface and associated proteins in FMRP-deficient neurons by quantitative mass spectrometry. Among them, we found increased steady-state levels of several subunits of the clathrin-adaptor protein complex 2 (AP-2), including AP2A1 and AP2B1.
2025-07-09 | PXD065502 | Pride
Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array
2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress
Project description:Characterizing the detergent insoluble brain proteome of sporadic late-onset Alzheimer’s disease (LOAD) has identified proteins and pathways associated with disease pathogenesis. Similar studies in early onset Alzheimer’s disease cases due to presenilin-1 mutations (PS1-EOAD), along with more detailed correlations with insoluble proteomes from LOAD and AD transgenic rodents, are limited. We therefore utilized quantitative proteomics to identify proteins that were significantly changing in the PS1-EOAD insoluble proteome versus controls. Comparison with the LOAD insoluble proteome identified common pathologic AD markers in addition to unique PS1-EOAD insoluble proteins. Similarly, weighted correlation network analysis (WGCNA) identified PS1-EOAD and LOAD co-expression modules with both like and disparate expression levels. Finally, we compared the human PS1-EOAD insoluble proteome to transgenic AD mouse and rat insoluble proteomes to understand how well these models mimic the human disease. Although many common AD pathologic findings were found in the rodents, there were multiple PS1-EOAD proteome changes not well recapitulated in the animal models. These proteomic studies highlight unique PS1-EOAD proteome changes as compared to LOAD and identify limitations to using AD transgenic rodents to study some aspects of AD.
2019-06-25 | PXD005321 | Pride
Project description:Histone H3 lysine 4 tri-methylation (H3K4me3) is a hallmark of transcription initiation, but how H3K4me3 is demethylated during gene repression is poorly understood. Jhd2, a JmjC domain protein, was recently identified as the major H3K4me3 histone demethylase (HDM) in S. cerevisiae. While JHD2 is required for removal of methylation upon gene repression, deletion of JHD2 does not result in increased levels of H3K4me3 in bulk histones, indicating that this HDM is unable to demethylate histones during steady state conditions. In this study, we showed that this was due to the negative regulation of Jhd2 activity by histone H3 lysine 14 acetylation, which co-localizes with H3K4me3 across the yeast genome. We demonstrated that loss of the histone H3-specific acetyltransferases (HATs) resulted in genome-wide-depletion of H3K4me3, and this was not due to a transcription defect. Moreover, H3K4me3 levels were reestablished in HAT mutants following loss of JHD2, which suggested that H3-specific HATs and Jhd2 served opposing functions in regulating H3K4me3 levels. We revealed the molecular basis for this suppression by demonstrating that histone H3K14 acetylation negatively regulated Jhd2 demethylase activity on an acetylated peptide in vitro. These results revealed the existence of a general mechanism for removal of H3K4me3 following gene repression. Examination of H3K4me3 in WT, ada2sas3, ada2sas3jhd2, and jhd2 strains.
2012-11-05 | E-GEOD-41424 | biostudies-arrayexpress
Project description:Characterizing the detergent insoluble brain proteome of sporadic late-onset Alzheimer’s disease (LOAD) has identified proteins and pathways associated with disease pathogenesis. Similar studies in early onset Alzheimer’s disease cases due to presenilin-1 mutations (PS1-EOAD), along with more detailed correlations with insoluble proteomes from LOAD and AD transgenic rodents, are limited. We therefore utilized quantitative proteomics to identify proteins that were significantly changing in the PS1-EOAD insoluble proteome versus controls. Comparison with the LOAD insoluble proteome identified common pathologic AD markers in addition to unique PS1-EOAD insoluble proteins. Similarly, weighted correlation network analysis (WGCNA) identified PS1-EOAD and LOAD co-expression modules with both like and disparate expression levels. Finally, we compared the human PS1-EOAD insoluble proteome to transgenic AD mouse and rat insoluble proteomes to understand how well these models mimic the human disease. Although many common AD pathologic findings were found in the rodents, there were multiple PS1-EOAD proteome changes not well recapitulated in the animal models. These proteomic studies highlight unique PS1-EOAD proteome changes as compared to LOAD and identify limitations to using AD transgenic rodents to study some aspects of AD. This submission exclusively provides the mouse and rat model data.
2022-03-01 | PXD005347 | Pride
Project description:Normal blood flow is essential for proper heart formation during embryonic development, as abnormal hemodynamic load (blood pressure and shear stress) results in cardiac defects seen in congenital heart disease. However, the progressive detrimental remodeling processes that relate altered blood flow to cardiac defects remain unclear. Outflow tract banding was used to increase hemodynamic load in the chicken embryo heart between Hamburger and Hamilton stages 18 and 24. Increased hemodynamic load induced increased cell density in outflow tract cushions, fewer cells along the endocardial lining, endocardium junction disruption, and altered periostin expression as measured by confocal microscopy analysis. Proteomic mass-spectrometry analysis quantified altered protein composition after banding.
2018-10-26 | PXD005362 | Pride
Project description:Right ventricular failure was induced thourgh pulmonary banding in 11 pigs. Right ventricular failure was defined as a SRVP >50 mmHg during two hours. After right ventricular failure was induced, half the pigs were treated with a Glenn-shunt combined with pulmonary banding for one hour, and the other half served as control group with pulmonary banding only. The aim was to study the change in global gene expression during right ventricular failure due to pulmonary banding, and the effect of volume unloading during pulmonary banding.
2013-06-11 | GSE47814 | GEO
Project description:It is becoming increasingly clear that individuals recovered from acute coronavirus disease 2019 (COVID-19) can develop into long-term sequelae termed ‘long coronavirus disease’ or ‘post-acute sequile SARS-CoV-2 infection’ (PACS). While most common manifestations of PACS are presented as systemic and long term, the early molecular mechanisms involved in the development of the sequelae remain elusive. To further understand immune responses globally after exposure to the virus, we surveyed plasma and saliva samples from COVID-19 and control - pre-pandemic- individuals. Initial serology investigation verified robust IgA and IgG responses with neutralizing activity to the SARS-CoV-2 and showed detection and positive correlations between paired plasma and saliva. To monitor immune pathways, we assayed our biofluids via shotgun proteomics. A dysbiosis in the proteomic profiles specially in persistent inflammatory patterns was detected in COVID-19 cases, revealing dysfunction of neutrophil-fibrinogen axis, relevant to immune and clotting functions. Overall our results reveal early dysbiotic immune markers, even when protective antibodies are found, demonstrating that serology is not sufficient to understand the health status. Additionally, we present saliva as a viable means to monitor serology, chronic inflammation and immune functions. Further delineation of the disease pathogenesis may provide biomarker and therapeutic targets to patients at risk to develop Post acute sequelae SARS-CoV-2 infection (PASC).
2025-06-25 | PXD033661 | Pride