Summary of Study ST002726
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.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
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.
| Study ID | ST002726 |
| Study Title | Metabolic and Proteomic Divergence is Present in Circulating Monocytes and Tissue Resident Macrophages from Berkeley Sickle Cell Anemia and B-thalassemia mice (Spleen) |
| Study Summary | Sickle 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 |
| Laboratory | Laboratory of Angelo D'Alessandro in collaboratation with David Irwin |
| Last Name | Cendali |
| First Name | Francesca |
| Address | 13199 East Montview Boulevard, Aurora, CO, 80045, USA |
| francesca.cendali@cuanschutz.edu | |
| Phone | 3037246131 |
| Submit Date | 2023-06-05 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2023-06-20 |
| Release Version | 1 |
Select appropriate tab below to view additional metadata details:
Factors:
Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)
| mb_sample_id | local_sample_id | Factor |
|---|---|---|
| SA273964 | 44 | Berk |
| SA273965 | 43 | Berk |
| SA273966 | 42 | Berk |
| SA273967 | 46 | Berk |
| SA273968 | 48 | Berk |
| SA273969 | 50 | Berk |
| SA273970 | 49 | Berk |
| SA273971 | 41 | Berk |
| SA273972 | 47 | Berk |
| SA273973 | 45 | Berk |
| SA273974 | 55 | Beta Thal |
| SA273975 | 54 | Beta Thal |
| SA273976 | 53 | Beta Thal |
| SA273977 | 56 | Beta Thal |
| SA273978 | 57 | Beta Thal |
| SA273979 | 60 | Beta Thal |
| SA273980 | 59 | Beta Thal |
| SA273981 | 58 | Beta Thal |
| SA273982 | 52 | Beta Thal |
| SA273983 | 51 | Beta Thal |
| SA273984 | 37 | WT |
| SA273985 | 38 | WT |
| SA273986 | 39 | WT |
| SA273987 | 31 | WT |
| SA273988 | 30 | WT |
| SA273989 | 36 | WT |
| SA273990 | 32 | WT |
| SA273991 | 33 | WT |
| SA273992 | 34 | WT |
| SA273993 | 35 | WT |
| SA273994 | 40 | WT |
| Showing results 1 to 31 of 31 |
