Summary of study ST001549

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001029. The data can be accessed directly via it's Project DOI: 10.21228/M8PM56 This work is supported by NIH grant, U2C- DK119886.

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Study IDST001549
Study Titleβ-Adrenergic regulation of metabolism in macrophages (part-III)
Study SummaryMacrophages have important roles in the immune system including clearing pathogens and wound healing. Metabolic phenotypes have been associated with functional phenotypes, where pro-inflammatory macrophages have an increased rate of glycolysis and anti-inflammatory macrophages primarily use oxidative phosphorylation. β-adrenoceptor (βAR) signalling in macrophages has been implicated in disease states such as cancer, atherosclerosis and rheumatoid arthritis. The impact of β-adrenoceptor signalling on macrophage metabolism has not been defined. Here we expand on defining the phenotype of macrophages treated with isoprenaline and describe the impact that βAR signalling has on the metabolome and proteome. We found that βAR signalling alters proteins involved in cytoskeletal rearrangement and redox control of the cell. We showed that βAR signalling in macrophages shifts glucose metabolism from glycolysis towards the tricarboxylic acid cycle and pentose phosphate pathways. We also show that βAR signalling perturbs purine metabolism by accumulating adenylate pools. Taken together these results indicate that βAR signalling shifts metabolism to support redox perturbations and upregulate proteins involved in cytoskeletal changes that may impact migration and phagocytosis processes.
Institute
Monash University
Last NamePeterson
First NameAmanda
AddressDrug delivery, disposition and dynamics, Pharmacy and Pharmaceutical Sciences, 381 Royal Parade, Parkville, Victoria, 3052, Australia
Emailamanda.peterson@monash.edu
Phone99039282
Submit Date2020-11-12
Raw Data AvailableYes
Raw Data File Type(s).raw
Analysis Type DetailLC-MS
Release Date2020-12-01
Release Version1
Amanda Peterson Amanda Peterson
https://dx.doi.org/10.21228/M8PM56
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR001029
Project DOI:doi: 10.21228/M8PM56
Project Title:β-Adrenergic regulation of metabolism in macrophages
Project Summary:Macrophages have important roles in the immune system including clearing pathogens and wound healing. Metabolic phenotypes have been associated with functional phenotypes, where pro-inflammatory macrophages have an increased rate of glycolysis and anti-inflammatory macrophages primarily use oxidative phosphorylation. β-adrenoceptor (βAR) signalling in macrophages has been implicated in disease states such as cancer, atherosclerosis and rheumatoid arthritis. The impact of β-adrenoceptor signalling on macrophage metabolism has not been defined. Here we expand on defining the phenotype of macrophages treated with isoprenaline and describe the impact that βAR signalling has on the metabolome and proteome. We found that βAR signalling alters proteins involved in cytoskeletal rearrangement and redox control of the cell. We showed that βAR signalling in macrophages shifts glucose metabolism from glycolysis towards the tricarboxylic acid cycle and pentose phosphate pathways. We also show that βAR signalling perturbs purine metabolism by accumulating adenylate pools. Taken together these results indicate that βAR signalling shifts metabolism to support redox perturbations and upregulate proteins involved in cytoskeletal changes that may impact migration and phagocytosis processes.
Institute:Monash University
Last Name:Peterson
First Name:Amanda
Address:Drug delivery, disposition and dynamics, Pharmacy and Pharmaceutical Sciences, 381 Royal Parade, Parkville, Victoria, 3052, Australia
Email:amanda.peterson@monash.edu
Phone:99039282
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