Summary of Study ST000560
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 PR000411. The data can be accessed directly via it's Project DOI: 10.21228/M8XG7R This work is supported by NIH grant, U2C- DK119886.
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| Study ID | ST000560 |
| Study Title | Metabolomics of immunoglobulin-producing cells in IgA nephropathy |
| Study Summary | IgA nephropathy (IgAN), the most common primary glomerulonephritis, is characterized by deposits of IgA-containing immune complexes in the kidney glomeruli, as first described by Berger and Hinglais in 1968. IgAN is a major cause of end-stage renal disease with its associated cardio-renal morbidity and mortality. Analyses of the IgA deposits revealed that the IgA is exclusively of the IgA1 subclass and that this IgA1 is aberrantly glycosylated, deficient in galactose in some O-glycans (Gd-IgA1). Patients with IgAN have elevated serum levels of Gd-IgA1 bound by anti-glycan autoantibodies in circulating immune complexes (CIC) that are fundamental in driving disease pathology in an autoimmune process. We have recently shown that elevated serum levels of Gd-IgA1 in patients with IgAN predict disease progression. Thus, understanding the mechanisms behind Gd-IgA1 production will improve future treatment options, as there is presently no disease-specific therapy. A total of 24 cell pellets (4 replicates from 6 cell lines) were analyzed by LCMS metabolomics. Immortalized immunoglobulin-producing cell lines were generated from peripheral-blood lymphocytes from patients with IgAN and healthy controls as described in Suzuki, H., Moldoveanu, Z., Hall, S., et al. IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1. J Clin Invest. 2008, 118, 629-639. |
| Institute | RTI International |
| Laboratory | NIH Eastern Regional Comphrehensive Metabolomics Resource Core at UNC Chapel Hill (ERCMRC) |
| Last Name | Sumner |
| First Name | Susan |
| Address | 3040 E. Cornwallis Road, Research Triangle Park, NC 27709 |
| susan_sumner@unc.edu | |
| Phone | 704-250-5000 |
| Submit Date | 2017-02-17 |
| Num Groups | 2 |
| Total Subjects | 24 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Waters) |
| Analysis Type Detail | LC-MS |
| Release Date | 2018-04-10 |
| Release Version | 1 |
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Project:
| Project ID: | PR000411 |
| Project DOI: | doi: 10.21228/M8XG7R |
| Project Title: | Metabolomics of immunoglobulin-producing cells in IgA nephropathy |
| Project Summary: | IgA nephropathy (IgAN), the most common primary glomerulonephritis, is characterized by deposits of IgA-containing immune complexes in the kidney glomeruli, as first described by Berger and Hinglais in 1968. IgAN is a major cause of end-stage renal disease with its associated cardio-renal morbidity and mortality. Analyses of the IgA deposits revealed that the IgA is exclusively of the IgA1 subclass and that this IgA1 is aberrantly glycosylated, deficient in galactose in some O-glycans (Gd-IgA1). Patients with IgAN have elevated serum levels of Gd-IgA1 bound by anti-glycan autoantibodies in circulating immune complexes (CIC) that are fundamental in driving disease pathology in an autoimmune process. We have recently shown that elevated serum levels of Gd-IgA1 in patients with IgAN predict disease progression. Thus, understanding the mechanisms behind Gd-IgA1 production will improve future treatment options, as there is presently no disease-specific therapy. A total of 24 cell pellets (4 replicates from 6 cell lines) were analyzed by LCMS metabolomics. Immortalized immunoglobulin-producing cell lines were generated from peripheral-blood lymphocytes from patients with IgAN and healthy controls as described in Suzuki, H., Moldoveanu, Z., Hall, S., et al. IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1. J Clin Invest. 2008, 118, 629-639. |
| Institute: | University of Alabama, Birmingham |
| Department: | Departments of Microbiology and Medicine |
| Last Name: | Novak |
| First Name: | Jan |
| Address: | 845 19th St.South, BBRB 761A |
| Email: | jannovak@uab.edu |
| Phone: | 205-934-4480 |
| Funding Source: | NIH/NIGMS Grant # K01GM109320 to Jessica Gooding; NIDDK Grant # K01DK106341 to Colin Reily; NIDDK Grant # DK078244 to Jan Novak and NIH Common Fund ERCMRC Grant # U24DK097193 to Susan Sumner |
| Contributors: | Jessica Gooding1,2, Colin Reily3, Courtney Whitaker1,2, Hieu Sy Vu1,2, Zach Acuff1,2, Susan McRitchie1,2, Bruce A. Julian3, Jan Novak3, Susan Sumner2,4 1Analytical Chemistry & Pharmaceutics, RTI International, RTP, NC 2NIH Eastern Regional Comprehensive Metabolomics Resource Core (ERCMRC) at UNC Chapel Hill, NC 3Departments of Microbiology and Medicine, University of Alabama at Birmingham, Birmingham, AL 4Nutrition Research Institute, University of North Carolina, Chapel Hill, NC |
