Evidence map›Paper›PMID 25624347›Full record

ArticleMolecular and cellular biology2015

Lysine-specific demethylase 2 suppresses lipid influx and metabolism in hepatic cells.

Katsuya Nagaoka, Shinjiro Hino, Akihisa Sakamoto, Kotaro Anan, Ryuta Takase, Takashi Umehara, Shigeyuki Yokoyama, Yutaka Sasaki, Mitsuyoshi Nakao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

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  14. Lysine-specific demethylase-2 is distinctively involved in brown and beige adipogenic differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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.

Katsuya NagaokaDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan Department of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Shinjiro HinoDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan s-hino@kumamoto-u.ac.jp mnakao@gpo.kumamoto-u.ac.jp.
Akihisa SakamotoDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Kotaro AnanDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Ryuta TakaseDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Takashi UmeharaRIKEN Systems and Structural Biology Center, Yokohama, Japan.
Shigeyuki YokoyamaRIKEN Systems and Structural Biology Center, Yokohama, Japan.
Yutaka SasakiDepartment of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Mitsuyoshi NakaoDepartment of Medical Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Tokyo, Japan s-hino@kumamoto-u.ac.jp mnakao@gpo.kumamoto-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells link environmental fluctuations, such as nutrition, to metabolic remodeling. Epigenetic factors are thought to be involved in such cellular processes, but the molecular basis remains unclear. Here we report that the lysine-specific demethylase 2 (LSD2) suppresses the flux and metabolism of lipids to maintain the energy balance in hepatic cells. Using transcriptome and chromatin immunoprecipitation-sequencing analyses, we revealed that LSD2 represses the genes involved in lipid influx and metabolism through demethylation of histone H3K4. Selective recruitment of LSD2 at lipid metabolism gene loci was mediated in part by a stress-responsive transcription factor, c-Jun. Intriguingly, LSD2 depletion increased the intracellular levels of many lipid metabolites, which was accompanied by an increased susceptibility to toxic cell damage in response to fatty acid exposure. Our data demonstrate that LSD2 maintains metabolic plasticity under fluctuating environment in hepatocytes by mediating the cross talk between the epigenome and metabolism.

Indexed as

Down-RegulationLipid MetabolismAnimalsHepatocytesHep G2 CellsHistone DemethylasesHistonesHumansLipidsLiverLysineMaleMethylationMice, Inbred C57BLProto-Oncogene Proteins c-junHistone DemethylasesHistonesKDM1B protein, humanLipidsLysineProto-Oncogene Proteins c-jun

Identifiers

PMID25624347
PMCPMC4355535

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.