Evidence map›Paper›PMID 24663349›Full record

ArticlePloS one2014

FOXO4-knockdown suppresses oxidative stress-induced apoptosis of early pro-angiogenic cells and augments their neovascularization capacities in ischemic limbs.

Takaharu Nakayoshi, Ken-Ichiro Sasaki, Hidemi Kajimoto, Hiroshi Koiwaya, Masanori Ohtsuka, Takafumi Ueno, Hidetoshi Chibana, Naoki Itaya, Masahiro Sasaki, Shinji Yokoyama and 2 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Takaharu NakayoshiDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Ken-Ichiro SasakiDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan; The Cardiovascular Research Institute, Kurume University, Fukuoka, Japan.
Hidemi KajimotoThe Cardiovascular Research Institute, Kurume University, Fukuoka, Japan.
Hiroshi KoiwayaDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Masanori OhtsukaDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Takafumi UenoDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Hidetoshi ChibanaDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Naoki ItayaDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Masahiro SasakiDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Shinji YokoyamaDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Yoshihiro FukumotoDivision of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Tsutomu ImaizumiInternational University of Health and Welfare, Fukuoka, Japan.
Kurume University · JPCardiovascular Institute Hospital · JPInternational University of Health and Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effects of therapeutic angiogenesis by intramuscular injection of early pro-angiogenic cells (EPCs) to ischemic limbs are unsatisfactory. Oxidative stress in the ischemic limbs may accelerate apoptosis of injected EPCs, leading to less neovascularization. Forkhead transcription factor 4 (FOXO4) was reported to play a pivotal role in apoptosis signaling of EPCs in response to oxidative stress. Accordingly, we assessed whether FOXO4-knockdown EPCs (FOXO4KD-EPCs) could suppress the oxidative stress-induced apoptosis and augment the neovascularization capacity in ischemic limbs. We transfected small interfering RNA targeted against FOXO4 of human EPCs to generate FOXO4KD-EPCs and confirmed a successful knockdown. FOXO4KD-EPCs gained resistance to apoptosis in response to hydrogen peroxide in vitro. Oxidative stress stained by dihydroethidium was stronger for the immunodeficient rat ischemic limb tissue than for the rat non-ischemic one. Although the number of apoptotic EPCs injected into the rat ischemic limb was greater than that of apoptotic EPCs injected into the rat non-ischemic limb, FOXO4KD-EPCs injected into the rat ischemic limb brought less apoptosis and more neovascularization than EPCs. Taken together, the use of FOXO4KD-EPCs with resistance to oxidative stress-induced apoptosis may be a new strategy to augment the effects of therapeutic angiogenesis by intramuscular injection of EPCs.

Indexed as

ApoptosisGene Knockdown TechniquesOxidative StressAdultAgedAnimalsCell Cycle ProteinsCytokinesFemaleForkhead Transcription FactorsGene Expression RegulationHindlimbHumansIschemiaMaleNeovascularization, PhysiologicCell Cycle ProteinsCytokinesForkhead Transcription FactorsFOXO4 protein, humanFOXO4 protein, ratReactive Oxygen SpeciesTranscription Factors

Identifiers

PMID24663349
PMCPMC3963928
OpenAlexW2041325378

What OpenQuestion holds

Textmetadata
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.