Evidence map›Paper›PMID 26041389›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2015

RTEF-1 protects against oxidative damage induced by H2O2 in human umbilical vein endothelial cells through Klotho activation.

Shan Sun, Bei Cheng, Pan-Ge Sun, Xiao-Hua Wu, Qin-Qin Wu, Ping He

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Klotho in Clinical Nephrology: Diagnostic and Therapeutic Implications.Clinical journal of the American Society of Nephrology : CJASN · 2020
    Review
  4. Review
  5. αKlotho and Chronic Kidney Disease.Vitamins and hormones · 2016
    Review
  6. 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

6 authors at 2 institutions in 1 country.

Shan SunDepartment of Gerontology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Bei ChengDepartment of Gerontology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Pan-Ge SunDepartment of Gerontology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Xiao-Hua WuDepartment of Gerontology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Qin-Qin WuDepartment of Gerontology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Ping HeDepartment of Gerontology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China doctorpeace74@gmail.com.
Huazhong University of Science and Technology · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is a main risk factor of vascular aging, which may lead to age-associated diseases. Related transcriptional enhancer factor-1 (RTEF-1) has been suggested to regulate many genes expression which are involved in the endothelial angiogenesis and vasodilation. However, whether RTEF-1 has a direct role in anti-oxidation and what specific genes are involved in RTEF-1-driven anti-oxidation have not been elucidated. In this study, we found that overexpressing RTEF-1 in H2O2-treated human umbilical vein endothelial cells decreased senescence-associated-β-galactosidase (SA-β-gal)-positive cells and G0/G1 cells population. The expressions of p53 and p21 were decreased in H2O2-treated RTEF-1 o/e human umbilical vein endothelial cells. However, specific small interfering RNA of RTEF-1 totally reversed the anti-oxidation effect of RTEF-1 and inhibited RTEF-1-induced decreased p53 and p21 expressions. It demonstrated that RTEF-1 could protect cells from H2O2-induced oxidative damage. In addition, we demonstrated that RTEF-1 could up-regulate Klotho gene expression and activate its promoter. Furthermore, Klotho small interfering RNA significantly blocked RTEF-1-driven endothelial cell protection from H2O2-induced oxidative damage and increased p53 and p21 expressions. These results reveal that RTEF-1 is a potential anti-oxidation gene and can prevent H2O2-induced endothelial cell oxidative damage by activating Klotho.

Indexed as

Blotting, WesternCellular SenescenceDNA-Binding ProteinsEndothelium, VascularGlucuronidaseHumansHydrogen PeroxideKlotho ProteinsMuscle ProteinsOncogene Protein p21(ras)Oxidative StressReal-Time Polymerase Chain ReactionRNA, Small InterferingTEA Domain Transcription FactorsTranscription FactorsTumor Suppressor Protein p53DNA-Binding ProteinsGlucuronidaseHydrogen PeroxideKlotho ProteinsMuscle ProteinsOncogene Protein p21(ras)RNA, Small InterferingTEAD4 protein, humanTEA Domain Transcription FactorsTranscription FactorsTumor Suppressor Protein p53humanKlothooxidative stressRelated transcriptional enhancer factor-1senescenceumbilical vein endothelial cells

Identifiers

PMID26041389
PMCPMC4935334
OpenAlexW2338151030

What OpenQuestion holds

Textmetadata
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.