Evidence map›Paper›PMID 27447109›Full record

ArticleCell death and differentiation2016

The miR-181d-regulated metalloproteinase Adamts1 enzymatically impairs adipogenesis via ECM remodeling.

S-Z Chen, L-F Ning, X Xu, W-Y Jiang, C Xing, W-P Jia, X-L Chen, Q-Q Tang, H-Y Huang

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

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  14. Fibroblast activation protein restrains adipogenic differentiation and regulates matrix-mediated mTOR signaling.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Fat fibrosis: friend or foe?JCI insight · 2018
    Review
  20. Article
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.

S-Z ChenDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
L-F NingDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
X XuInstitute of Stem Cell Research and Regenerative Medicine, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
W-Y JiangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
C XingDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
W-P JiaDepartment of Endocrinology and Metabolism, Shanghai Clinical Center for Diabetes, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
X-L ChenDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, Saint Paul, MN 55108, USA.
Q-Q TangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
H-Y HuangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Fudan University · CNMinistry of Education of the People's Republic of China · CNAssociated Colleges of the Twin Cities · USShanghai Sixth People's Hospital · CN

Funding

Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1995 to 2015
$17.0M
NIDDK NIH HHS P30 DK050456
6 · The paper itself

Abstract

The extracellular matrix (ECM) maintenance is crucial to the structural integrity of adipocytes and whole adipose tissue formation. However, the potential impact of the ECM on adipocyte lineage commitment is unclear. Herein, we demonstrate that forced expression of matrix-associated metalloproteinase Adamts1 (a disintegrin and metalloproteinase with thrombospondin motifs 1), which we show is targeted by microRNA-181d (miR-181d) during BMP4-induced adipocytic lineage commitment, markedly impairs adipocyte commitment. Conversely, siRNA-induced inhibition of Adamts1 promotes adipocyte commitment. Adamst1 metalloprotease activity is required for this inhibition and is determined to function via remodeling ECM components followed by activating FAK-ERK signaling pathway during the commitment process. Furthermore, ablation of Adamts1 in adipose tissue increases adipose tissue mass, reduces insulin sensitivity, and disrupts lipid homeostasis. This finding is consistent with Adamts1 decreased expression in the adipose tissue of obese mice and an inverse correlation of Adamts1 expression with body mass index in humans. Collectively, our results indicate that Adamts1 acts as an ECM 'modifier', with miR-181d-induced downregulation, that regulates adipocyte lineage commitment and obesity.

Indexed as

AdipogenesisADAMTS1 ProteinAdipocytesAdipose TissueAdultAnimalsBase SequenceBone Morphogenetic Protein 4Cell LineageExtracellular MatrixExtracellular Signal-Regulated MAP KinasesHomeostasisHumansMice, Inbred C57BLMicroRNAsMiddle AgedADAMTS1 ProteinBone Morphogenetic Protein 4Extracellular Signal-Regulated MAP KinasesMicroRNAsMIrn181 microRNA, humanmirn181 microRNA, mouse

Identifiers

PMID27447109
PMCPMC5071569
OpenAlexW2498342930

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.