Evidence map›Paper›PMID 27512010›Full record

ArticleJournal of lipid research2016

CXCL3 positively regulates adipogenic differentiation.

Joji Kusuyama, Anna Komorizono, Kenjiro Bandow, Tomokazu Ohnishi, Tetsuya Matsuguchi

Abstract read
In one paragraph

Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  18. Bone Marrow Adiposity in Models of Radiation- and Aging-Related Bone Loss Is Dependent on Cellular Senescence.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
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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

5 authors.

Joji KusuyamaDepartment of Oral Biochemistry, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Anna KomorizonoDepartment of Oral Biochemistry, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Kenjiro BandowDepartment of Oral Biology and Tissue Engineering, Meikai University School of Dentistry, Saitama, Japan.
Tomokazu OhnishiDepartment of Oral Biochemistry, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Tetsuya MatsuguchiDepartment of Oral Biochemistry, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. Electronic address: tmatsugu@dent.kagoshima-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines are a family of cytokines inducing cell migration and inflammation. Recent reports have implicated the roles of chemokines in cell differentiation. However, little is known about the functional roles of chemokines in adipocytes. Here, we explored gene expression levels of chemokines and chemokine receptors during adipogenic differentiation. We have found that two chemokines, chemokine (C-X-C motif) ligand 3 (CXCL3) and CXCL13, as well as CXC chemokine receptor 2 (CXCR2), a CXCL3 receptor, are highly expressed in mature adipocytes. When 3T3-L1 cells and ST2 cells were induced to differentiate, both the number of lipid droplets and the expression levels of adipogenic markers were significantly promoted by the addition of CXCL3, but not CXCL13. Conversely, gene knockdown of either CXCL3 or CXCR2 by specific siRNA effectively inhibited the course of adipogenic differentiation. CXCL3 treatment of 3T3-L1 cells significantly induced the phosphorylation of ERK and c-jun N-terminal kinase (JNK). Furthermore, CXCL3-induced CCAAT-enhancer binding protein (C/EBP)β and δ expression was suppressed by both ERK and JNK-specific inhibitors. Furthermore, chromatin immunoprecipitation assay revealed functional binding of PPARγ2 within the cxcl3 promoter region. Taken together, these results have indicated that CXCL3 is a novel adipokine that facilitates adipogenesis in an autocrine and/or a paracrine manner through induction of c/ebpb and c/ebpd.

Indexed as

3T3-L1 CellsAdipogenesisAdipokinesAnimalsCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding Protein-deltaCell DifferentiationChemokine CXCL13Chemokines, CXCExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMiceParacrine CommunicationPPAR gammaPromoter Regions, GeneticAdipokinesCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding Protein-deltaCebpb protein, mouseCebpd protein, mouseChemokine CXCL13Chemokines, CXCCxcl13 protein, mouseCxcl3 protein, mouseExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesPPAR gammaReceptors, Interleukin-8BadipocyteschemokineC-X-C motif chemokine ligand 3cytokinesinflammationperoxisome proliferator-activated receptorsprotein kinases/mitogen-activated protein kinase

Identifiers

PMID27512010
PMCPMC5036360

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.