Evidence map›Paper›PMID 20947660›Full record

ArticleHuman molecular genetics2011

Dystrophin conferral using human endothelium expressing HLA-E in the non-immunosuppressive murine model of Duchenne muscular dystrophy.

Chang-Hao Cui, Shunichiro Miyoshi, Hiroko Tsuji, Hatsune Makino, Seiichi Kanzaki, Daisuke Kami, Masanori Terai, Harumi Suzuki, Akihiro Umezawa

Open access · hybridAbstract read
In one paragraph

Article in Human molecular genetics, 2011. 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
0.8field-weighted citation impact, top 28% 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, 12 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Chang-Hao CuiDepartment of Reproductive Biology, National Institute for Child Health and Development, Tokyo, Japan.
Shunichiro Miyoshi
Hiroko Tsuji
Hatsune Makino
Seiichi Kanzaki
Daisuke Kami
Masanori Terai
Harumi Suzuki
Akihiro Umezawa
National Center For Child Health and Development · JPKeio University · JPMudanjiang Medical University · CNSaitama International Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human leukocyte antigen (HLA)-E is a non-classical major histocompatibility complex class I (Ib) molecule, which plays an important role in immunosuppression. In this study, we investigated the immunomodulating effect of HLA-E in a xenogeneic system, using human placental artery-derived endothelial (hPAE) cells expressing HLA-E in a mouse model. In vitro cell lysis analysis by primed lymphocytes in combination with siRNA transfection showed that HLA-E is necessary for inhibition of the immune response. Similarly, in vivo cell implantation analysis with siRNA-mediated down-regulation of HLA-E demonstrates that HLA-E is involved in immunosuppression. As hPAE cells efficiently transdifferentiate into myoblasts/myocytes in vitro, we transplanted the cells into mdx mice, a model of Duchenne muscular dystrophy. hPAE cells conferred dystrophin to myocytes of the 'immunocompetent' mdx mice with extremely high efficiency. These findings suggest that HLA-E-expressing cells with a myogenic potential represent a promising source for cell-based therapy of patients with muscular dystrophy.

Indexed as

Endothelial CellsAnimalsArteriesCell Culture TechniquesDisease Models, AnimalDystrophinGene Expression RegulationHistocompatibility Antigens Class IHLA-E AntigensHumansImmunocompetenceMiceMice, Inbred BALB CMice, Inbred mdxMuscle DevelopmentMuscular Dystrophy, DuchenneDystrophinHistocompatibility Antigens Class IHLA-E AntigensRNA, Small Interfering

Identifiers

PMID20947660
PMCPMC3005899
OpenAlexW2131524695

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.