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Proteomic profile of macrophage serectome

ABSTRACT: Macrophage secretome- Macrophages were isolated from the left ventricle from control (day 0) or from the infarct region at day 1 after myocardial infarction (MI). Cells were isolated in RPMI media with 0.1% fetal bovine serum and incubated for 2 hours and then spun at 800g for 5 min to separate cell debris. The sample sizes are n=4 biological replicates for each time point.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart, Macrophage

SUBMITTER: Elizabeth Flynn

LAB HEAD: Merry Lindsey

PROVIDER: PXD011780 | Pride | 2022-05-19

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	14240142411449214494D06.msf	Msf
	14240142411449214494D06.raw	Raw
	144411444214444G1D03.msf	Msf
	144411444214444G1D03.raw	Raw
	144451448414485G3D07.msf	Msf

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1 - 5 of 18

Publications

Macrophages secrete murinoglobulin-1 and galectin-3 to regulate neutrophil degranulation after myocardial infarction.

Chalise Upendra U Daseke Michael J MJ Kalusche William J WJ Konfrst Shelby R SR Rodriguez-Paar Jocelyn R JR Flynn Elizabeth R ER Cook Leah M LM Becirovic-Agic Mediha M Lindsey Merry L ML

Molecular omics 20220328 3

Inflammation presides early after myocardial infarction (MI) as a key event in cardiac wound healing. Ischemic cardiomyocytes secrete inflammatory cues to stimulate infiltration of leukocytes, predominantly macrophages and neutrophils. Infiltrating neutrophils degranulate to release a series of proteases including matrix metalloproteinase (MMP)-9 to break down extracellular matrix and remove necrotic myocytes to create space for the infarct scar to form. While neutrophil to macrophage communicat ...[more]

PMID: 35230372

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Fibroblast secretome proteomic analysis

Project description:LV fibroblasts were isolated from control (day 0), and infarcted regions at day 1, day 3, and day 7 after myocardial infarction (MI). Cells were isolated in DMEM in 10% fetal bovine serum and were seeded into 6-well plates and were allowed to grow to 80% confluence in DMEM supplemented with 10% fetal bovine serum (FBS). Cells were serum starved (DMEM + 0.1% FBS) for 18 h and then media was changed and secretome was collected after 24 h. The sample sizes are n=3 biological replicates for each time point.

2019-10-25 | PXD011778 | Pride

Tc1 and Tc2 secretion proteome evaluation

Project description:The goal of this project is to dissect the mechanism by which Tc1 and Tc2 effector subtypes effect cell physiology in vitro. I utilized cellular proteomics to determine Tc1 and Tc2 secretion patterns and identify inflammatory factors that regulate cell polarization and physiology in vitro.

2022-02-15 | PXD011757 | Pride

Arhgef11 high and low salt kidney proteomic analysis

Project description:Arhgef11 is a Rho guanine nucleotide exchange factor previously implicated in kidney injury in the Dahl salt-sensitive rat (SS-WT). Through exchange of GDP for GTP, Arhgef11 regulates cytoskeletal structure, function, and cell-cell contacts through a variety of stimuli (e.g., G-protein coupled receptors, growth factors, and shear stress). We studied the SS-Arhgef11-/- rat model at 4-12 weeks of age under low and high salt (0.3% or 2% NaCl). To better understand the molecular mechanisms associated with renal protection from loss of Arhgef11, MS/MS proteomics was performed on kidney from SS-Arhgef11-/- and SS-WT at week 12 (low-salt). At week 12, 1017 genes and 363 proteins were observed. In summary, in vivo phenotyping provides strong evidence that increased Arhgef11 expression in the Dahl S rat leads to actin cytoskeleton mediated changes in cell morphology and cell function (impaired reuptake filtered protein) that promote kidney injury, hypertension, and decline in kidney function.

2021-09-08 | PXD011758 | Pride

Proteomics of JHS samples identifies proteins associated with heart failure

Project description:RELEVANCE: Identifying early plasma protein biomarkers that predict the development of heart failure (HF) following myocardial infarction (MI) will help to stratify at risk subjects and provide insight into more effective therapeutic strategies. OBJECTIVE/HYPOTHESIS: The goal of this study was to determine markers of HF in African Americans, using plasma samples collected before the development of symptoms. We propose that early plasma glycoprotein changes will link to later development of heart failure. ApolipoproteinF will be the strongest indicator. METHODS: Plasma samples from a subset of Jackson Heart Study participants with a history of MI but without prevalent heart failure (HF) at visit 2 (2005-2008) were analyzed by glycoproteomics. Individuals were grouped into those who experienced subsequent HF hospitalization after visit 2 (n=15; 3 men/ 12 women) and those without HF hospitalization through 2012 (n=45; 24 men/ 21 women). N-linked plasma glycopeptides were quantified by solid-phase extraction coupled to mass spectrometry and identified using RefSeq and SwissProt. Proteins were mapped for biological processes and functional pathways using Ingenuity Pathway Analysis (IPA) and linked to clinical characteristics.

2018-08-30 | PXD009870 | Pride

Woundhealing proteomic profile

Project description:Glycoproteomics was performed on plasma collected from mice 3 days after biopsy punch wound healing and 3 days after myocardial infarction (MI) wound healing.

2022-04-01 | PXD011790 | Pride

Consequences of fibroblast ablation in adult murine hearts

Project description:Fibroblasts produce the majority of collagen in the heart and are thought to regulate extracellular matrix (ECM) turnover. However, the in vivo role of fibroblasts in structuring the basal ECM network is poorly understood. To examine the effects of fibroblast loss on the microenvironment in the adult murine heart, we generated mice with reduced fibroblast numbers and evaluated the tissue microenvironment during homeostasis and after injury. We determined that a 60-80% reduction in fibroblasts numbers did not overtly change the fibrillar collagen network but did alter the distribution and abundance of type VI collagen, a microfibrillar collagen that forms an open network with the basement membrane. In fibroblast ablated mice, myocardial infarction did not result in ventricular wall rupture, and heart function was more effectively preserved during angiotensin II/phenylephrine (AngII/PE) induced fibrosis. Analysis of cardiomyocyte contractility demonstrated weaker contractions and slower calcium release and reuptake in uninjured and AngII/PE infused fibroblast ablated animals. Moreover, fibroblast ablated hearts have a similar gene expression prolife to hearts with exercise-induced and physiological hypertrophy after AngII/PE infusion. These results suggest that hearts are resilient to a significant degree of fibroblast loss and that fibroblasts can directly impact cardiomyocyte function. Furthermore, a reduction in fibroblasts may have cardioprotective effects heart after injury suggesting that manipulation of the number of fibroblasts may have therapeutic value.

2023-03-10 | PXD021741 | Pride

Data in support of administration of a soluble TNF inhibitor that reduces infarct volume after focal cerebral ischemia in mice

Project description:Background: Tumor necrosis factor, which exists both as a soluble (solTNF) and a transmembrane (tmTNF) protein, plays an important role in post-stroke inflammation. The objective of the present study was to test the effect of topical versus intracerebroventricular administration of XPro1595 (a solTNF inhibitor) and etanercept (a solTNF and tmTNF inhibitor) compared to saline on output measures such as infarct volume and post-stroke inflammation in mice. Methods: Adult male C57BL/6 mice were treated topically (2.5 mg/ml/1µl/hr for 3 consecutive days) or intracerebroventricularly (1.25 mg/kg/0.5 ml, once) with saline, XPro1595, or etanercept immediately after permanent middle cerebral artery occlusion (pMCAO). Mice were allowed to survive 1 or 3 days. Infarct volume, microglial and leukocyte profiles, and inflammatory markers were evaluated. Results: We found that topical, and not intracerebroventricular, administration of XPro1595 reduced infarct volume at both 1 day and 3 days after pMCAO. Etanercept showed no effect. We observed no changes in microglial or leukocyte populations. XPro1595 increased gene expression of P2ry12 at 1 day and Trem2 at 1 and 3 days, while decreasing Cx3cr1 expression at 1 and 3 days after pMCAO, suggesting a change in microglial activation towards a phagocytic phenotype. Conclusions: Our data demonstrate that topical administration of XPro1595 for three consecutive days decreases infarct volumes after ischemic stroke, while modifying microglial activation and the inflammatory response post-stroke. This suggests that inhibitors of solTNF hold great promise for future neuroprotective treatment in ischemic stroke.

2019-11-12 | PXD014440 | Pride

Expression data from C57BL/6J and MRL/MpJ hearts following acute myocardial infarction

Project description:The Murphy Roth Large (MRL) mouse, a strain capable of regenerating right ventricular myocardium, has a high post-myocardial infarction (MI) survival rate compared with C57BL6/J (C57) mice. The biological processes responsible for this survival advantage are unknown. We compared acute post-MI gene expression in C57 and MRL hearts using microarrays and identified promising candidate biological processes underlying increased survival in the MRL. Hearts from both strains were excised at different time points before or after MI for RNA extraction and hybridization to MOE430A arrays. Baseline hearts were excised from healthy mice that had not undergone the MI procedure (day 0). Infarct tissue in this case means tissue taken from the anterior-apical region that would be the infarct region in a post-MI heart. Non-infarct covers the remainder of the LV. Post-MI hearts were excised either 1 or 5 days after MI. We had successful hybridizations for 3 replicates each of C57 day 0 infarct and non-infarct tissue (6 arrays), 4 MRL day 0 infarct and non-infarct tissue (8 arrays), 4 C57 day 1 infarct and non-infarct tissue (8 arrays), 4 MRL day 1 infarct and non-infarct tissue (8 arrays), 4 C57 day 5 infarct and non-infarct tissue (8 arrays), and 4 MRL day 5 infarct and non-infarct tissue (8 arrays).

2010-05-27 | E-GEOD-19322 | biostudies-arrayexpress

Integrative proteomic and phosphoproteomics analysis of human ischemic and dilated cardiomyopathic explant tissues identifies etiology-specific phosphorylation patterns and signaling pathways

Project description:Myocardial tissue samples were explanted from the explanted left ventricle of heart failure patients with DCM (n=4), left ventricular infarct, peri-, and non-infarct regions of HF patients with ICM (n=4) at the time of their heart transplant surgeries, and the left ventricle of age- and sex-matched non-failing controls (NFC, n=4). Comparative quantitative analysis was performed on three independent sets (DCM vs. NFC, infarct vs. non-infarct, and peri- vs. non-infarct) labeled with 10-plex tandem mass tags. Following enrichment of phosphorylated peptides, the flow-through and eluted fractions were collected separately and subjected to LC-MS/MS (liquid chromatography-tandem mass spectrometry) on a Q-Exactive HF for global proteomics and phosphoproteomics profiling respectively.

2023-11-20 | PXD012664 | Pride

Reanalysis of Pandey lab's draft of the human proteome

Project description:The availability of human genome sequence has transformed biomedical research over the past decade. However, an equivalent map for the human proteome with direct measurements of proteins and peptides was lacking. To this end, Akhilesh Pandey's lab reported a draft map of the human proteome based on high resolution Fourier transform mass spectrometry-based proteomics technology, which included an in-depth proteomic profiling of 30 histologically normal human samples including 17 adult tissues, 7 fetal tissues and 6 purified primary hematopoietic cells ( http://dx.doi.org/10.1038/nature13302 ). The profiling resulted in identification of proteins encoded by greater than 17,000 genes accounting for ~84% of the total annotated protein-coding genes in humans. This large human proteome catalog (available as an interactive web-based resource at http://www.humanproteomemap.org) complements available human genome and transcriptome data to accelerate biomedical research in health and disease. Pandey's lab and collaborators request that those considering use of this primary dataset for commercial purposes contact pandey@jhmi.edu. The full details of this study can be found in the PRIDE database: www.ebi.ac.uk/pride/archive/projects/PXD000561/. This ArrayExpress entry represents a top level summary of the metadata only which formed the basis of the reanalysis performed by Joyti Choudhary's team ( jc4@sanger.ac.uk ), results of which are presented in the Expression Atlas at EMBL-EBI : http://www.ebi.ac.uk/gxa/experiments/E-PROT-1.

2015-03-10 | E-PROT-1 | biostudies-arrayexpress

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