Summary of Study ST002727

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, 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.


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.
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
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 application/zip

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Treatment ID:TR002842
Treatment Summary:Eight- to ten-week-old female C57Bl/6 WT, Berk-ss, or Hbbth3/+ mice were either obtained from Jackson Laboratories (Bar Harbor, ME, USA) or our in-house Berk SCD mouse colony. Mice were housed and bred in an AAALAC accredited animal facility at the University of Colorado, Denver, Anschutz Medical campus and were maintained on a 12:12 light-dark cycle with food and water available ad libitum. Female heterozygous Berk-ss mice were bred with male homozygous Berkss mice to generate homozygous offspring. Specifically, Berk-ss mice with genotype Tg(HuminiLCR α1 Gγ Aγ δ βs ) Hba0/0 Hbb0/0 and the hemizygous with genotype Tg(Hu-miniLCR α1 Gγ Aγ δ βs ) Hba0/0 Hbb0 Hbb+ were littermates. Genotyping of mice used for breeding and experiments was performed by TransnetYX (Cordova, TN, USA). A total of 21 mice (C57Bl/6: n=10, Berk-ss mice: n=11, Hbbth3/+ =10) were used in the present investigation and levels of discomfort and distress were monitored daily by the in-house animal care staff, with a veterinarian available as needed. All experimental procedures were conducted under the guidelines recommended by The Journal of Physiology (11), the National Institutes of Health and were approved by the Institutional Animal Care and Use Committee at the University of Colorado, Denver, Anschutz Medical Campus.