Label-Free Quantitative Proteomic Profiling of LAD2 Mast Cell Releasates
Ontology highlight
ABSTRACT: Tween-80 is one of the most important causes resulting in anaphylactoid reaction. However, its mechanism remains unclear. A Label-free LCMS/MS-based proteomics was used to analyze Tween-80-stimulated LAD2 mast cell releasates. Out of a total dataset of 2546 proteins, 882 proteins were found in the supernate samples of Tween-80-treated LAD2 mast cells; 313 proteins were up-expressed and 111 proteins were down-expressed. KEGG pathway analysis showed that endocytosis was the largest class of pathway. A total of 52 proteins were involved in endocytosis, and mainly related to G-protein-coupled receptor (GPCR)-endocytosis and EGFR-endocytosis. Cell adhesion molecules (CAMs) pathway was the most significant differences, with a total of 21 proteins involved. NF-κB signaling activation and calcium signaling pathway play an important role in Tween-80-induced LAD2 cells activation. Proteins, including tyrosine-protein kinase, PLCγ, PKCβ, and p50/p65, were mainly involved in NF-κB pathways. NF-κB signaling activation mainly involved in tyrosine-protein kinase, PLCγ, PKCβ, and NF-κB p50/p65. Calcium signaling pathway mainly related to PLCγ/PKC PLCγ/STIM1 mediated store-operated calcium entry (SOCE) and PLCγ mediated store-operated calcium entry (SOCE)PLCγ/PKC pathway. These results suggest that Tween-80 might be internalized via GPCR-endocytosis, which induces degranulation by SOCE PLCγ/PKC or SOCE PLCγ/PKC pathways mediated calcium influx, and promotes the generation of inflammatory mediators and CAMs via NF-κB signaling pathway finally resulting in anaphylactoid reaction.
ORGANISM(S): Homo Sapiens
SUBMITTER: Yongxiao Cao
PROVIDER: PXD016123 | iProX | Mon Nov 04 00:00:00 GMT 2019
REPOSITORIES: iProX
ACCESS DATA