Evidence map›Paper›PMID 25860801›Full record

ArticlePloS one2015

Melanocortins contribute to sequential differentiation and enucleation of human erythroblasts via melanocortin receptors 1, 2 and 5.

Eriko Simamura, Tomohiro Arikawa, Takayuki Ikeda, Hiroki Shimada, Hiroki Shoji, Hiroko Masuta, Yuriko Nakajima, Hiroki Otani, Hideto Yonekura, Toshihisa Hatta

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
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  9. Melanocortin 5 receptor signaling pathway in health and disease.Cellular and molecular life sciences : CMLS · 2020
    Review
  10. Article
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  13. 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

10 authors at 2 institutions in 1 country.

Eriko SimamuraDepartment of Anatomy, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Tomohiro ArikawaDepartment of Biology, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Takayuki IkedaDepartment of Biochemistry, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Hiroki ShimadaDepartment of Anatomy, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Hiroki ShojiDepartment of Biology, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Hiroko MasutaDepartment of Anatomy, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Yuriko NakajimaDepartment of Anatomy, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Hiroki OtaniDepartment of Developmental Biology, Faculty of Medicine, Shimane University, Izumo 693-8601, Japan.
Hideto YonekuraDepartment of Biochemistry, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University School of Medicine, Uchinada, Ishikawa 920-0293, Japan.
Kanazawa Medical University · JPShimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we showed that adrenocorticotropic hormone (ACTH) promoted erythroblast differentiation and increased the enucleation ratio of erythroblasts. Because ACTH was contained in hematopoietic medium as contamination, the ratio decreased by the addition of anti-ACTH antibody (Ab). Addition of neutralizing Abs (nAbs) for melanocortin receptors (MCRs) caused erythroblast accumulation at specific stages, i.e., the addition of anti-MC2R nAb led to erythroblast accumulation at the basophilic stage (baso-E), the addition of anti-MC1R nAb caused accumulation at the polychromatic stage (poly-E), and the addition of anti-MC5R nAb caused accumulation at the orthochromatic stage (ortho-E). During erythroblast differentiation, ERK, STAT5, and AKT were consecutively phosphorylated by erythropoietin (EPO). ERK, STAT5, and AKT phosphorylation was inhibited by blocking MC2R, MC1R, and MC5R, respectively. Finally, the phosphorylation of myosin light chain 2, which is essential for the formation of contractile actomyosin rings, was inhibited by anti-MC5R nAb. Taken together, our study suggests that MC2R and MC1R signals are consecutively required for the regulation of EPO signal transduction in erythroblast differentiation, and that MC5R signal transduction is required to induce enucleation. Thus, melanocortin induces proliferation and differentiation at baso-E, and polarization and formation of an actomyosin contractile ring at ortho-E are required for enucleation.

Indexed as

Adrenocorticotropic HormoneAntibodies, NeutralizingCell DifferentiationCells, CulturedErythroblastsErythropoiesisExtracellular Signal-Regulated MAP KinasesHumansMelanocortinsModels, BiologicalProto-Oncogene Proteins c-aktReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 2Receptors, MelanocortinSignal TransductionSTAT5 Transcription FactorAdrenocorticotropic HormoneAntibodies, NeutralizingExtracellular Signal-Regulated MAP Kinasesmelanocortin 5 receptorMelanocortinsProto-Oncogene Proteins c-aktReceptor, Melanocortin, Type 1Receptor, Melanocortin, Type 2Receptors, MelanocortinSTAT5 Transcription Factor

Identifiers

PMID25860801
PMCPMC4393082
OpenAlexW2049223396

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.