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NPRA-deficient mice cardiac tissue LC-MS/MS

ABSTRACT: For this part, we analyzed 10 samples, which were two biological replicates for each NPRA-deficient mice and the matched littermate. The experimental system was designed for 10-plex tandem mass tag (TMT)-based mass spectrometry analysis.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Yan Niu

LAB HEAD: Jun Yu

PROVIDER: PXD020997 | Pride | 2021-04-26

REPOSITORIES: pride

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Publications

Integrative Proteomic and Metabolomic Analysis Reveals Metabolic Phenotype in Mice With Cardiac-Specific Deletion of Natriuretic Peptide Receptor A.

Chang Pan P Niu Yan Y Zhang Xiaomeng X Zhang Jing J Wang Xihui X Shen Xi X Chen Baoying B Yu Jun J

Molecular & cellular proteomics : MCP 20210331

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are important biological markers and cardiac function regulators. Natriuretic peptide receptor A (NPRA) binds to an ANP or BNP ligand and induces transmembrane signal transduction by elevating the intracellular cyclic guanosine monophosphate (cGMP) levels. However, the metabolic phenotype and related mechanisms induced by NPRA deletion remain ambiguous. Here, we constructed myocardial-specific NPRA deletion mice and detected th ...[more]

PMID: 33812089

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Human vitreous TMT labelled LC-MS/MS

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iTRAQ-based quantitative serum proteomic analysis in ischemic stroke patients

Project description:Hemorrhagic transformation (HT), which occurs with or without reperfusion treatments (thrombolysis and/or thrombectomy), deteriorates the outcomes of ischemic stroke patients. It is essential to find clinically reliable biomarkers that can predict HT. In this study, we screened for potential serum biomarkers from an existing blood bank and database with 243 suspected acute ischemic stroke (AIS) patients. A total of 37 patients were enrolled, who were diagnosed as AIS but did not receive reperfusion treatment. They were divided into two groups based on whether they accompanied with HT or not (5 HT and 32 non-HT). Serum samples were labeled by isobaric tags for relative and absolute quantitation (iTRAQ) and analyzed by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) and compared under NCBInr database. A total of 647 proteins in sera samples were captured and the levels of 17 proteins (12 up-regulated and 5 down-regulated) were significantly different. These differentially expressed proteins were further categorized with Gene Ontology functional classification annotation and Kyoto Encyclopedia of Genes and Genomes metabolic pathway analysis into biological processes. Further protein-protein interaction analysis using String database discovered that, among the differential expressed proteins, 10 pairs of proteins were found to have crosstalk connections, which may have direct (physical) and indirect (functional) interactions for the development of HT. Our findings suggest that these differentially expressed proteins could serve as potential biomarkers for predicting HT after ischemic stroke.

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Differences in proteins between normal and asthmatic mice and effects of knockout TL1A on asthmatic mice

Project description:Asthma, a heterogeneous disease, is characterized by chronic inflammation, epithelial–mesenchymal transformation (EMT), and airway remodeling. After immune system activation, macrophages, T cells, and other cells gather and secrete various factors, such as interleukin-1β, 4, 5, 10, 13, and TNF-a, which break the anti-inflammatory balance and aggravate the progression of asthma. TNF-a, a member of the TNF superfamily, has promising future in the pathophysiological progress of autoimmune diseases and the development and application of related drugs. However, the mechanisms of TNF-a in mucus secretion, airway hyperreactivity, and airway remodeling of human asthma remains unclear. Tumor necrosis factor-like cytokine 1A is a type II transmembrane protein with a stable trimer structure similar to TNF-a. Migone et al. first uncovered the presence of TL1A as a membrane-bound protein (mTL1A) or a soluble protein (sTL1A) from mTL1A cleaved by an underlying enzyme. DR3 is a type I membrane protein that contains a death domain in the cytoplasmic region and remains highly homologous with other TNFRSF members. Interestingly, Evangelos et al. found that TNF-a-stimulated human lung myofibroblasts significantly increase TL1A expression and collagen production. Our study will identify the specific role of TNF-a-stimulated mTL1A/DR3 or sTL1A/DR3 axis in the EMT of asthma model.

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Quantitative Proteomics Reveals the Dynamic Pathophysiology across Different Stages in a Rat Model of Severe Traumatic Brain Injury

Project description:Background: Severe Traumatic Brain Injury (TBI) has become a growing health problem, causing a vast society burden worldwide. However, characteristic mechanisms between acute and subacute stages have not been systemically revealed. Methods: Sixty rats were randomly divided into sham surgery and model groups. Severe TBI model was induced by controlled cortical impact (CCI). Neurological deficits were evaluated by modified neurological severity score (mNSS). H&E staining and immunofluorescence were performed to assess the injured brain tissues. The protein expressions of hippocampus were analyzed by the tandem mass tag-based (TMT) quantitative proteomics on the third and fourteenth days. The shared and stage-specific differentially expressed proteins (DEPs) were screened, and then analyzed by the gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG) and protein-protein interaction (PPI). Eventually, target proteins were further verified by Western blotting (WB). Results: The neurological deficits always exist from the acute stage to the subacute stage of severe TBI and showed a downward trend. The brain parenchyma of TBI models was dramatically impaired. A total of 375 and 139 DEPs were identified at day 3 and 14, respectively. Sixty-three DEPs were co-existed between the two stages. Both stages were mainly related to the complement and coagulation cascades pathway. Three pathways associated with gastric acid secretion, insulin secretion and thyroid hormone synthesis were only enriched in the acute phase. Comparatively, amyotrophic lateral sclerosis (ALS) was significantly enriched in the subacute stage. WB confirmed the reliability of the TMT quantitative proteomics results. Conclusion: Our findings highlight the same and different pathological processes in the acute and subacute phases of severe TBI and provide potential protein biomarkers.

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AKT/PACS2 participates in renal vascular hyperpermeability by regulating endothelial fatty acid oxidation in diabetic mice

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