TY - DATA T1 - Proteome profiling in IL-1β and VEGF-activated human umbilical vein endothelial cells delineates the interlink between inflammation and angiogenesis PY - 2017/06/15 AU - Thomas Mohr AU - Verena Haudek-Prinz AU - Astrid Slany AU - Johannes Grillari AU - Michael Micksche AU - Christopher Gerner UR - https://plos.figshare.com/articles/dataset/Proteome_profiling_in_IL-1_and_VEGF-activated_human_umbilical_vein_endothelial_cells_delineates_the_interlink_between_inflammation_and_angiogenesis/5111902 DO - 10.1371/journal.pone.0179065 L4 - https://ndownloader.figshare.com/files/8685802 L4 - https://ndownloader.figshare.com/files/8685808 L4 - https://ndownloader.figshare.com/files/8685814 KW - Obtained protein profiles KW - VEGF KW - GPI KW - gene co-expression analysis KW - HSPG KW - inflammation KW - GO-Term enrichment analysis KW - map kinases MAP 2K Weighted protein co-expression network analysis KW - CST KW - NOD KW - ANXA KW - CXCL KW - HUVEC KW - angiogenesis Endothelial cells KW - LC-MS KW - Term enrichment analysis KW - IL KW - hub genes N2 - Endothelial cells represent major effectors in inflammation and angiogenesis, processes that drive a multitude of pathological states such as atherosclerosis and cancer. Both inflammation and angiogenesis are interconnected with each other in the sense that many pro-inflammatory proteins possess proangiogenic properties and vice versa. To elucidate this interplay further, we present a comparative proteome study of inflammatory and angiogenic activated endothelial cells. HUVEC were stimulated with interleukin 1-β and VEGF, respectively. Cultured primary cells were fractionated into secreted, cytoplasmic and nuclear protein fractions and processed for subsequent LC-MS/MS analysis. Obtained protein profiles were filtered for fraction-specific proteins to address potential cross fractional contamination, subjected to comparative computational biology analysis (GO-Term enrichment analysis, weighted gene co-expression analysis) and compared to published mRNA profiles of IL-1β respectively VEGF stimulated HUVEC. GO Term enrichment analysis and comparative pathway analysis revealed features such as NOD and NfkB signaling for inflammatory activated HUVEC and VEGF and ErB signaling for VEGF-activated HUVEC with potential crosstalk via map kinases MAP2K2. Weighted protein co-expression network analysis revealed several potential hub genes so far not associated with driver function in inflammation or angiogenesis such as HSPG2, ANXA3, and GPI. “Classical” inflammation or angiogenesis markers such as IL6, CXCL8 or CST1 were found in a less central position within the co-expression networks. In conclusion, this study reports a framework for the computational biology based analysis of proteomics data applied to cytoplasmic, nucleic and extracellular fractions of quiescent, inflammatory and angiogenic activated HUVEC. Novel potential hub genes relevant for these processes were successfully identified. ER -