title: Riboflavin deficiency induces a significant change in proteomic profiles in HepG2 cells.
abstract: Riboflavin deficiency is widespread in many regions over the world, especially in underdeveloped countries. In this study, we investigated the effects of riboflavin deficiency on protein expression profiles in HepG2 cells in order to provide molecular information for the abnormalities induced by riboflavin deficiency. HepG2 cells were cultured in media containing different concentrations of riboflavin. Changes of cell viability and apoptosis were assessed. A comparative proteomic analysis was performed using a label-free shotgun method with LC-MS/MS to investigate the global changes of proteomic profiles in response to riboflavin deficiency. Immunoblotting test was used to validate the results of proteomic approach. The cell viability and apoptosis tests showed that riboflavin was vital in maintaining the cytoactivity of HepG2 cells. The label-free proteomic analysis revealed that a total of 37 proteins showing differential expression (±2 fold, p < 0.05) were identified after riboflavin deficiency. Bioinformatics analysis indicated that the riboflavin deficiency caused an up-regulation of Parkinson's disease pathway, steroid catabolism, endoplasmic reticulum stress and apoptotic process, while the fatty acid metabolism, tricarboxylic citrate cycle, oxidative phosphorylation and iron metabolism were down-regulated. These findings provide a molecular basis for the elucidation of the effects caused by riboflavin deficiency.
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.|School of Public Health, Guangxi Medical University, Nanning, 530021, China.
authors.forename: Zhonghao
authors.initials: Z
authors.lastname: Xin
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.
authors.forename: Lingling
authors.initials: L
authors.lastname: Pu
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.
authors.forename: Weina
authors.initials: W
authors.lastname: Gao
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.|School of Public Health, Guangxi Medical University, Nanning, 530021, China.
authors.forename: Yawen
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.
authors.forename: Jingyu
authors.initials: J
authors.lastname: Wei
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.
authors.forename: Tala
authors.initials: T
authors.lastname: Shi
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.
authors.forename: Zhanxin
authors.initials: Z
authors.lastname: Yao
authors.affiliation: Institute of Health and Environmental Medicine, Tianjin, 300050, China.
authors.forename: Changjiang
authors.initials: C
authors.lastname: Guo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002470:Cell Survival / Q000235:genetics; D056945:Hep G2 Cells; D006801:Humans; D050356:Lipid Metabolism / Q000235:genetics; D010300:Parkinson Disease / Q000235:genetics* / Q000473:pathology; D020543:Proteome / Q000235:genetics; D012256:Riboflavin / Q000235:genetics*; D012257:Riboflavin Deficiency / Q000235:genetics* / Q000473:pathology; D015398:Signal Transduction / Q000235:genetics
chemical_list: D020543:Proteome; D012256:Riboflavin