Evidence map›Paper›PMID 27151674›Full record

ArticleScientific reports2016

3H-1,2-dithiole-3-thione protects retinal pigment epithelium cells against Ultra-violet radiation via activation of Akt-mTORC1-dependent Nrf2-HO-1 signaling.

Ke-Ran Li, Su-Qing Yang, Yi-Qing Gong, Hong Yang, Xiu-Miao Li, Yu-Xia Zhao, Jin Yao, Qin Jiang, Cong Cao

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Article
  2. Review
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  9. Article
  10. The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging.Oxidative medicine and cellular longevity · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
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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

9 authors.

Ke-Ran LiInstitute of Neuroscience, Soochow University, Suzhou, Jiangsu 215021, China.
Su-Qing YangInstitute of Neuroscience, Soochow University, Suzhou, Jiangsu 215021, China.
Yi-Qing GongThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing 210029, China.
Hong YangThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiu-Miao LiThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing 210029, China.
Yu-Xia ZhaoThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing 210029, China.
Jin YaoThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing 210029, China.
Qin JiangThe Affiliated Eye Hospital of Nanjing Medical University, Nanjing 210029, China.
Cong CaoInstitute of Neuroscience, Soochow University, Suzhou, Jiangsu 215021, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive UV radiation and reactive oxygen species (ROS) cause retinal pigment epithelium (RPE) cell injuries. Nrf2 regulates transcriptional activation of many anti-oxidant genes. Here, we tested the potential role of 3H-1,2-dithiole-3-thione (D3T) against UV or ROS damages in cultured RPE cells (both primary cells and ARPE-19 line). We showed that D3T significantly inhibited UV-/H2O2-induced RPE cell death and apoptosis. UV-stimulated ROS production was dramatically inhibited by D3T pretreatment. D3T induced Nrf2 phosphorylation in cultured RPE cells, causing Nrf2 disassociation with KEAP1 and its subsequent nuclear accumulation. This led to expression of antioxidant response elements (ARE)-dependent gene heme oxygenase-1 (HO-1). Nrf2-HO-1 activation was required for D3T-mediated cytoprotective effect. Nrf2 shRNA knockdown or S40T dominant negative mutation as well as the HO-1 inhibitor Zinc protoporphyrin (ZnPP) largely inhibited D3T's RPE cytoprotective effects against UV radiation. Yet, exogenous overexpression Nrf2 enhanced D3T's activity in RPE cells. Further studies showed that D3T activated Akt/mTORC1 in cultured RPE cells. Akt-mTORC1 inhibitors, or Akt1 knockdown by shRNA, not only inhibited D3T-induced Nrf2-HO-1 activation, but also abolished the RPE cytoprotective effects. In vivo, D3T intravitreal injection protected from light-induced retinal dysfunctions in mice. Thus, D3T protects RPE cells from UV-induced damages via activation of Akt-mTORC1-Nrf2-HO-1 signaling axis.

Indexed as

Ultraviolet RaysAnimalsApoptosisCells, CulturedHeme Oxygenase-1HumansMechanistic Target of Rapamycin Complex 1Membrane ProteinsMice, Inbred C57BLNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktRadiation-Protective AgentsReactive Oxygen SpeciesRetinal Pigment EpitheliumSignal TransductionThiones1,2-dithiol-3-thioneHeme Oxygenase-1Hmox1 protein, mouseMechanistic Target of Rapamycin Complex 1Membrane ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktRadiation-Protective AgentsReactive Oxygen SpeciesThionesThiophenes

Identifiers

PMID27151674
PMCPMC4858705

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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.