Evidence map›Paper›PMID 24402046›Full record

ArticleThe Journal of investigative dermatology2014

BNIP3 plays crucial roles in the differentiation and maintenance of epidermal keratinocytes.

Mariko Moriyama, Hiroyuki Moriyama, Junki Uda, Akifumi Matsuyama, Masatake Osawa, Takao Hayakawa

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 58 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

6 authors at 3 institutions in 1 country.

Mariko MoriyamaPharmaceutical Research and Technology Institute, Kinki University, Higashi-Osaka, Osaka, Japan; Platform for Realization of Regenerative Medicine, Foundation for Biomedical Research and Innovation, Kobe, Hyogo, Japan.
Hiroyuki MoriyamaPharmaceutical Research and Technology Institute, Kinki University, Higashi-Osaka, Osaka, Japan. Electronic address: mariko@phar.kindai.ac.jp.
Junki UdaPharmaceutical Research and Technology Institute, Kinki University, Higashi-Osaka, Osaka, Japan.
Akifumi MatsuyamaPlatform for Realization of Regenerative Medicine, Foundation for Biomedical Research and Innovation, Kobe, Hyogo, Japan.
Masatake OsawaDivision of Regeneration Technology, Gifu University School of Medicine, Gifu, Gifu, Japan.
Takao HayakawaPharmaceutical Research and Technology Institute, Kinki University, Higashi-Osaka, Osaka, Japan.
Kindai University · JPFoundation for Biomedical Research and Innovation · JPGifu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptome analysis of the epidermis of Hes1(-/-) mouse revealed the direct relationship between Hes1 (hairy and enhancer of split-1) and BNIP3 (BCL2 and adenovirus E1B 19-kDa-interacting protein 3), a potent inducer of autophagy. Keratinocyte differentiation is going along with activation of lysosomal enzymes and organelle clearance, expecting the contribution of autophagy in this process. We found that BNIP3 was expressed in the suprabasal layer of the epidermis, where autophagosome formation is normally observed. Forced expression of BNIP3 in human primary epidermal keratinocytes (HPEKs) resulted in autophagy induction and keratinocyte differentiation, whereas knockdown of BNIP3 had the opposite effect. Intriguingly, addition of an autophagy inhibitor significantly suppressed the BNIP3-stimulated differentiation of keratinocytes, suggesting that BNIP3 plays a crucial role in keratinocyte differentiation by inducing autophagy. Furthermore, the number of dead cells increased in the human epidermal equivalent of BNIP3 knockdown keratinocytes, which suggests that BNIP3 is important for maintenance of skin epidermis. Interestingly, although UVB irradiation stimulated BNIP3 expression and cleavage of caspase3, suppression of UVB-induced BNIP3 expression led to further increase in cleaved caspase3 levels. This suggests that BNIP3 has a protective effect against UVB-induced apoptosis in keratinocytes. Overall, our data provide valuable insights into the role of BNIP3 in the differentiation and maintenance of epidermal keratinocytes.

Indexed as

Gene Expression RegulationAnimalsApoptosisAutophagyBasic Helix-Loop-Helix ProteinsCaspase 3Cell DifferentiationCell LineEpidermisGene Expression Regulation, EnzymologicHomeodomain ProteinsHomeostasisHumansKeratinocytesLysosomesMembrane ProteinsBasic Helix-Loop-Helix ProteinsBNIP3 protein, humanBNip3 protein, mouseCaspase 3Hes1 protein, mouseHomeodomain ProteinsMembrane ProteinsMicroRNAsMitochondrial ProteinsProto-Oncogene ProteinsTranscription Factor HES-1

Identifiers

PMID24402046
OpenAlexW2081394823

What OpenQuestion holds

Textmetadata
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.