Evidence map›Paper›PMID 28901450›Full record

ArticleMolecular medicine reports2017

Role of hypoxia‑mediated cellular prion protein functional change in stem cells and potential application in angiogenesis (Review).

Seung Pil Yun, Yong-Seok Han, Jun Hee Lee, Yeo Min Yoon, Chul Won Yun, Peter Rhee, Sang Hun Lee

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. 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 at 4 institutions in 2 countries.

Seung Pil YunDepartment of Neurology, Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Yong-Seok HanDepartment of Biochemistry, Medical Science Research Institute, Soonchunhyang University College of Medicine, Cheonan, South Chungcheong 31151, Republic of Korea.
Jun Hee LeeDepartment of Pharmacology and Toxicology, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294, USA.
Yeo Min YoonDepartment of Biochemistry, Medical Science Research Institute, Soonchunhyang University College of Medicine, Cheonan, South Chungcheong 31151, Republic of Korea.
Chul Won YunDepartment of Biochemistry, Medical Science Research Institute, Soonchunhyang University College of Medicine, Cheonan, South Chungcheong 31151, Republic of Korea.
Peter RheeDepartment of Neurology, Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Sang Hun LeeDepartment of Biochemistry, Medical Science Research Institute, Soonchunhyang University College of Medicine, Cheonan, South Chungcheong 31151, Republic of Korea.
Soonchunhyang University · KRJohns Hopkins Medicine · USJohns Hopkins University · USUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular prion protein (PrPC) can replace other pivotal molecules due to its interaction with several partners in performing a variety of important biological functions that may differ between embryonic and mature stem cells. Recent studies have revealed major advances in elucidating the putative role of PrPC in the regulation of stem cells and its application in stem cell therapy. What is special about PrPC is that its expression may be regulated by hypoxia‑inducible factor (HIF)‑1α, which is the transcriptional factor of cellular response to hypoxia. Hypoxic conditions have been known to drive cellular responses that can enhance cell survival, differentiation and angiogenesis through adaptive processes. Our group recently reported hypoxia‑enhanced vascular repair of endothelial colony‑forming cells on ischemic injury. Hypoxia‑induced AKT/signal transducer and activator of transcription 3 phosphorylation eventually increases neovasculogenesis. In stem cell biology, hypoxia promotes the expression of growth factors. According to other studies, aspects of tissue regeneration and cell function are influenced by hypoxia, which serves an essential role in stem cell HIF‑1α signaling. All these data suggest the possibility that hypoxia‑mediated PrPC serves an important role in angiogenesis. Therefore, the present review summarizes the characteristics of PrPC, which is produced by HIF‑1α in hypoxia, as it relates to angiogenesis.

Indexed as

Cell HypoxiaEmbryonic Stem CellsGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitNeovascularization, PathologicOncogene Protein v-aktPrion ProteinsSignal TransductionHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitOncogene Protein v-aktPrion Proteins

Identifiers

PMID28901450
PMCPMC5865755
OpenAlexW2753401345

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.