Summary of Study ST002727

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 PR001691. The data can be accessed directly via it's Project DOI: 10.21228/M84B0K This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002727
Study TitleMetabolic and Proteomic Divergence is Present in Circulating Monocytes and Tissue Resident Macrophages from Berkeley Sickle Cell Anemia and B-thalassemia mice (Liver)
Study SummarySickle cell disease and Beta-thalassemia represent hemoglobinopathies arising from dysfunctional or under produced beta-globin chains, respectively. In both diseases, red blood cell injury and anemia are the impetus for end organ injury. Because persistent erythrophagocytosis is a hallmark of these genetic maladies it is critical to understand how macrophage phenotype polarizations in tissue compartments can inform on disease progression. Murine models of sickle cell disease and Beta-thalassemia allow for a basic understanding of mechanisms and provide for translation to human disease. A multi-omics approach to understanding macrophage metabolism and protein changes in two murine models of beta-globinopathy was performed on peripheral blood mononuclear cells as well as spleen and liver macrophages isolated from Berkley sickle cell disease (Berk-ss) and heterozygous B1/B2 globin gene deletion (Hbbth3/+) mice. Results from these experiments revealed the metabolome and proteome of macrophages are polarized to a distinct phenotype in Berk-ss and Hbbth3/+ compared each other and their common background mice (C57BL6/J). Further, spleen and liver macrophages revealed distinct disease specific phenotypes, suggesting macrophages become differentially polarized and reprogrammed within tissue compartments. We conclude that tissue recruitment, polarization, metabolic and proteomic reprogramming of macrophages in Berk-ss and Hbbth3/+ mice may be relevant to disease to progression in other tissue.
Institute
University of Colorado School of Medicine
LaboratoryLaboratory of Angelo D'Alessandro in collaboratation with David Irwin
Last NameCendali
First NameFrancesca
Address13199 East Montview Boulevard, Aurora, CO, 80045, USA
Emailfrancesca.cendali@cuanschutz.edu
Phone3037246131
Submit Date2023-06-05
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2023-06-20
Release Version1
Francesca Cendali Francesca Cendali
https://dx.doi.org/10.21228/M84B0K
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Collection:

Collection ID:CO002826
Collection Summary:Whole blood samples (1 mL) were obtained from animals via cardiac puncture, using a syringe with a 26-gauge needle, and placed in an EDTA treated tube. The blood was transferred to a 15 mL conical tube and diluted 2:1, sterile PBS: blood, and gently mixed. Lympholyte® Mammal Cell Separation media (Cedarlane Labs, product # CL5115) was gently added to the bottom of the blood solution and spun at 1400 rpm for 30 minutes in a refrigerated centrifuge. After centrifugation, layers were visualized, the PBMC layer (midlayer) was extracted and resuspended in a new tube. The isolated PBMC’s were washed using ~14mL sterile PBS, spun at 1800 rpm for 10 minutes, excess PBS was removed, cells were resuspended in 1-2mL for counting, and the final pellet was frozen in liquid nitrogen and stored at -80C.
Sample Type:Macrophages
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