Peptide-based systems analysis of inflammation induced myeloid-derived suppressor cells reveals diverse signaling pathways

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dc.contributor.authorChoksawangkarn, Waeowalee
dc.contributor.authorGraham, Lauren M.
dc.contributor.authorBurke, Meghan
dc.contributor.authorLee, Sang Bok
dc.contributor.authorOstrand-Rosenberg, Suzanne
dc.contributor.authorFenselau, Catherine
dc.contributor.authorEdwards, Nathan J.
dc.date.accessioned2019-03-05T19:37:34Z
dc.date.available2019-03-05T19:37:34Z
dc.date.issued2016-05-19
dc.description.abstractA better understanding of molecular signaling between myeloid-derived suppressor cells (MDSC), tumor cells, T-cells, and inflammatory mediators is expected to contribute to more effective cancer immunotherapies. We focus on plasma membrane associated proteins, which are critical in signaling and intercellular communication, and investigate changes in their abundance in MDSC of tumor-bearing mice subject to heightened versus basal inflammatory conditions. Using spectral counting, we observed statistically significant differential abundances for 35 proteins associated with the plasma membrane, most notably the pro-inflammatory proteins S100A8 and S100A9 which induce MDSC and promote their migration. We also tested whether the peptides associated with canonical pathways showed a statistically significant increase or decrease subject to heightened versus basal inflammatory conditions. Collectively, these studies used bottom-up proteomic analysis to identify plasma membrane associated pro-inflammatory molecules and pathways that drive MDSC accumulation, migration, and suppressive potency.en_US
dc.description.sponsorshipThis research was supported by a grant from the National Institutes of Health, GM 021248. S.B.L. also thanks to the WCU program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology, R31–2008- 000–10071-0. W.C. acknowledges a Royal Thai Government Fellowship. We acknowledge the support of the Maryland NanoCenter and its NispLab. The NispLab is supported in part by the National Science Foundation as an MRSEC Shared Experimental Facility.en_US
dc.description.urihttps://onlinelibrary.wiley.com/doi/full/10.1002/pmic.201500102en_US
dc.format.extent15 pagesen_US
dc.genrejournal articles postprintsen_US
dc.identifierdoi:10.13016/m2rkgz-fdsk
dc.identifier.citationWaeowalee Choksawangkarn, Lauren M. Graham, et.al, Peptide‐based systems analysis of inflammation induced myeloid‐derived suppressor cells reveals diverse signaling pathways, PROTEOMICS, Volume 16, Issue 13, DOI : https://doi.org/10.1002/pmic.201500102en_US
dc.identifier.urihttps://doi.org/10.1002/pmic.201500102
dc.identifier.urihttp://hdl.handle.net/11603/12936
dc.language.isoen_USen_US
dc.publisherJohn Wiley & Sonsen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Biological Sciences Department Collection
dc.relation.ispartofUMBC Faculty Collection
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
dc.rightsThis is the peer reviewed version of the following article: Waeowalee Choksawangkarn, Lauren M. Graham, et.al, Peptide‐based systems analysis of inflammation induced myeloid‐derived suppressor cells reveals diverse signaling pathways, PROTEOMICS, Volume 16, Issue 13, DOI : https://doi.org/10.1002/pmic.201500102, which has been published in final form at https://doi.org/10.1002/pmic.201500102. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.
dc.subjectcell migrationen_US
dc.subjectdifferential protein expressionen_US
dc.subjectimmune suppressionen_US
dc.subjectinflammationen_US
dc.subjectmass spectrometry – LC-MS/MSen_US
dc.subjectmyeloid-derived suppressor cellsen_US
dc.subjectsystems biologyen_US
dc.titlePeptide-based systems analysis of inflammation induced myeloid-derived suppressor cells reveals diverse signaling pathwaysen_US
dc.typeTexten_US

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