Evidence map›Paper›PMID 24217227›Full record

ArticleInternational journal of molecular sciences2013

The protective effect of Bcl-xl overexpression against oxidative stress-induced vascular endothelial cell injury and the role of the Akt/eNOS pathway.

Leng Ni, Tianjia Li, Bao Liu, Xitao Song, Genhuan Yang, Linfang Wang, Shiying Miao, Changwei Liu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2013. 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
1.1field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. HJournal of nanobiotechnology · 2022
    Article
  4. Bcl-xL as a Modulator of Senescence and Aging.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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 at 2 institutions in 1 country.

Leng NiDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Peking Union Medical College, 1# Shuaifuyuan, Dongcheng District, Beijing 100730, China. liucw@vip.sina.com.
Tianjia Li
Bao Liu
Xitao Song
Genhuan Yang
Linfang Wang
Shiying Miao
Changwei Liu
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking Union Medical College Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Restenosis after intraluminal or open vascular reconstruction remains an important clinical problem. Vascular endothelial cell (EC) injury induced by oxidative stress plays an important role in the development of intimal hyperplasia. In this study, we sought to evaluate the protective effects of Bcl-xl overexpression in vitro on oxidative stress-induced EC injury and the role of the Akt/endothelial nitric oxide synthase (eNOS) pathway. Human umbilical vein endothelial cells (HUVECs) exposed to hydrogen peroxide (H2O2, 0.5 mM) were used as the experimental oxidative stress model. The Bcl-xl gene was transferred into HUVECs through recombinant adenovirus vector pAdxsi-GFP-Bcl-xl before oxidative treatment. Cell apoptosis was evaluated by Annexin V/propidium iodide and Hoechst staining, caspase-7 and PARP cleavage. Cell viability was assessed using the cell counting kit-8 assay, proliferating cell nuclear antigen (PCNA) immunocytochemical detection and the scratching assay. Expressions of Akt, phospho-Akt and eNOS were detected by Western blotting. Our results showed that H2O2 induced apoptosis and decreased the cell viability of HUVECs. Bcl-xl overexpression significantly protected cells from H2O2-induced cell damage and apoptosis and maintained the cell function. Furthermore, the level of phospho-Akt and eNOS protein expression was significantly elevated when pretreated with Bcl-xl gene transferring. These findings suggest that Bcl-xl overexpression exerts an anti-apoptotic and protective effect on EC function. The Akt/eNOS signaling pathway is probably involved in these processes.

Indexed as

Oxidative StressApoptosisbcl-X ProteinCoronary RestenosisEndothelial CellsGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsHydrogen PeroxideNitric Oxide Synthase Type IIIOncogene Protein v-aktSignal TransductionBCL2L1 protein, humanbcl-X ProteinHydrogen PeroxideNitric Oxide Synthase Type IIIOncogene Protein v-akt

Identifiers

PMID24217227
PMCPMC3856057
OpenAlexW2109017650

What OpenQuestion holds

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LicenceCC BY
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.