Cargando…

Phosphorylated proteomics analysis of human coronary artery endothelial cells stimulated by Kawasaki disease patients serum

BACKGROUND: Kawasaki disease (KD) is an acute febrile childhood systemic vasculitis that disturbs coronary arteries. The pathogenesis remains unknown. The study of phosphorylated proteins helps to elucidate the relevant pathophysiological mechanisms of cardiovascular disease. However, few researches...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Shui-Ming, Liu, Wan-Ting, Yang, Fang, Yi, Qi-Jian, Zhang, Shuai, Jia, Hong-Ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6337789/
https://www.ncbi.nlm.nih.gov/pubmed/30654760
http://dx.doi.org/10.1186/s12872-018-0982-2
Descripción
Sumario:BACKGROUND: Kawasaki disease (KD) is an acute febrile childhood systemic vasculitis that disturbs coronary arteries. The pathogenesis remains unknown. The study of phosphorylated proteins helps to elucidate the relevant pathophysiological mechanisms of cardiovascular disease. However, few researches explored phosphorylated proteins in KD patients. METHODS: We compared phosphoprotein profiles of HCAECs stimulated by the serum of KD patients and normal children using iTRAQ technology, TiO(2) enrichment phosphorylated peptide and MS analysis. Then we conducted the functional analysis by ClueGO and the biological interaction networking analysis by ReactomeFIViz. Western blotting was performed to identify the hub proteins. RESULTS: Our results revealed that phosphorylation of 148 proteins showed different intensities between the two HCAECs groups, which are enriched in MAPK, VEGFR, EGFR, Angiopoietin receptor, mTOR, FAK signaling pathway and so on. Through the Network Analyzer analysis, the hub proteins are CDKN1A, MAPK1 and POLR2A, which were experimentally validated. CONCLUSION: In summary, we provided evidence addressing the valuable phosphorylation signaling that could be useful resource to understand the molecular mechanism and the potential targets for novel therapy of KD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12872-018-0982-2) contains supplementary material, which is available to authorized users.