Evidence map›Paper›PMID 28765965›Full record

ArticleMolecular medicine reports2017

Downregulation of SMP30 in senescent human lens epithelial cells.

Shuning Li, Xi Chen, Weixia Lai, Meixia Hu, Xin Zhong, Shaojian Tan, Hao Liang

Abstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Cellular senescence: a view throughout organismal life.Cellular and molecular life sciences : CMLS · 2018
    Review
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

7 authors.

Shuning LiDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Xi ChenDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Weixia LaiDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Meixia HuDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Xin ZhongDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Shaojian TanDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Hao LiangDepartment of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescence marker protein 30 (SMP30) has been reported to serve antiapoptotic and antioxidant roles, as well as roles in Ca2+ regulation, and may be involved in the occurrence and development of cataract. The present study aimed to investigate the expression of SMP30 in senescent human lens epithelial cells (HLECs) and explored the relationship between SMP30 and aging. SRA01/04 cells, a HLEC line, were treated with H2O2 to mimic aging, and cell morphological changes were observed by microscopy and cell activity was exami-ned by MTT assay, senescence‑associated‑β‑galactosidase (SA‑β‑Gal) staining and cell cycle analysis. The expression of SMP30 mRNA and protein was measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting. Following prolonged low‑dose H2O2 exposure, cells exhibited senescence‑related morphological changes, reduced growth activity, increased SA‑β‑Gal positive staining and cell cycle arrest in the S and G2/M phases. SMP30 mRNA expression levels were significantly downregulated following exposure to 75 and 100 µM H2O2, and the protein expression levels in the same groups were decreased by >6‑fold compared with the control untreated cells. However, no significant change was observed in SMP30 expression in the 25 and 50 µM H2O2 exposure groups. These results suggest that, in the early stage of senescence induced by H2O2‑mediated chronic oxidative stress, there may be no significant change in SMP30 expression, but when the oxidative stress increases and senescence is aggravated, SMP30 may be significantly downregulated in the senescent HLECs. The present study indicates that SMP30 may be an important factor involved in the aging process of HLECs and the development of cataract.

Indexed as

Gene Expression RegulationApoptosisBiomarkersCalcium-Binding ProteinsCataractCell CycleCell LineCell SurvivalCellular SenescenceEpithelial CellsHumansHydrogen PeroxideIntracellular Signaling Peptides and ProteinsLens, CrystallineOxidative StressTime FactorsBiomarkersCalcium-Binding ProteinsHydrogen PeroxideIntracellular Signaling Peptides and ProteinsRGN protein, human

Identifiers

PMID28765965
PMCPMC5646983

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.