Evidence map›Paper›PMID 28367977›Full record

ArticleScientific reports2017

Riboflavin deficiency induces a significant change in proteomic profiles in HepG2 cells.

Zhonghao Xin, Lingling Pu, Weina Gao, Yawen Wang, Jingyu Wei, Tala Shi, Zhanxin Yao, Changjiang Guo

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Proteomic Landscape of Adeno-Associated Virus (AAV)-Producing HEK293 Cells.International journal of molecular sciences · 2021
    Article
  11. Review
  12. Article
  13. Review
  14. Gut Vibes in Parkinson's Disease: The Microbiota-Gut-Brain Axis.Movement disorders clinical practice · 2019
    Review
  15. Article
  16. Flavin homeostasis in the mouse retina during aging and degeneration.The Journal of nutritional biochemistry · 2018
    Article
  17. Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Zhonghao XinInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Lingling PuInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Weina GaoInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Yawen WangInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Jingyu WeiInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Tala ShiInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Zhanxin YaoInstitute of Health and Environmental Medicine, Tianjin, 300050, China.
Changjiang GuoInstitute of Health and Environmental Medicine, Tianjin, 300050, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsApoptosisCell SurvivalHep G2 CellsHumansLipid MetabolismParkinson DiseaseProteomeRiboflavinRiboflavin DeficiencySignal TransductionProteomeRiboflavin

Identifiers

PMID28367977
PMCPMC5377456

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.