Evidence map›Paper›PMID 29799877›Full record

ArticlePloS one2018

Aortic carboxypeptidase-like protein enhances adipose tissue stromal progenitor differentiation into myofibroblasts and is upregulated in fibrotic white adipose tissue.

Mike Jager, Mi-Jeong Lee, Chendi Li, Stephen R Farmer, Susan K Fried, Matthew D Layne

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 28 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 1 institution in 1 country.

Mike JagerDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Mi-Jeong LeeSection of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Chendi LiDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Stephen R FarmerDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Susan K FriedSection of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Matthew D LayneDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, United States of America.ORCID 0000-0003-0007-4870
Boston University · US

Funding

Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
TRAINING PROGRAM IN ENDOCRINE AND METABOLIC RESEARCHT32DK007201 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CORKEY, BARBARA E., KANDROR, KONSTANTIN V · 1986 to 2023
$6.4M
Glucocorticoids & Adipocyte Function in Human ObesityR01DK080448 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIED, SUSAN K · 2009 to 2018
$3.4M
NIDDK NIH HHS P30 DK046200NIDDK NIH HHS R01 DK080448NIDDK NIH HHS T32 DK007201
6 · The paper itself

Abstract

White adipose tissue expands through both adipocyte hypertrophy and hyperplasia and it is hypothesized that fibrosis or excess accumulation of extracellular matrix within adipose tissue may limit tissue expansion contributing to metabolic dysfunction. The pathways that control adipose tissue remodeling are only partially understood, however it is likely that adipose tissue stromal and perivascular progenitors participate in fibrotic remodeling and also serve as adipocyte progenitors. The goal of this study was to investigate the role of the secreted extracellular matrix protein aortic carboxypeptidase-like protein (ACLP) on adipose progenitor differentiation in the context of adipose tissue fibrosis. Treatment of 10T1/2 mouse cells with recombinant ACLP suppressed adipogenesis and enhanced myofibroblast differentiation, which was dependent on transforming growth factor-β receptor kinase activity. Mice fed a chronic high fat diet exhibited white adipose tissue fibrosis with elevated ACLP expression and cellular fractionation of these depots revealed that ACLP was co-expressed with collagens primarily in the inflammatory cell depleted stromal-vascular fraction (SVF). SVF cells isolated from mice fed a high fat diet secreted increased amounts of ACLP compared to low fat diet control SVF. These cells also exhibited reduced adipogenic differentiation capacity in vitro. Importantly, differentiation studies in primary human adipose stromal cells revealed that mature adipocytes do not express ACLP and exogenous ACLP administration blunted their differentiation potential while upregulating myofibroblastic markers. Collectively, these studies identify ACLP as a stromal derived mediator of adipose progenitor differentiation that may limit adipocyte expansion during white adipose tissue fibrosis.

Indexed as

Up-RegulationAdipose TissueAdipose Tissue, WhiteAnimalsCarboxypeptidasesCell DifferentiationCells, CulturedFibrosisHumansMaleMiceMyofibroblastsReceptors, Transforming Growth Factor betaRepressor ProteinsStromal CellsAEBP1 protein, humanCarboxypeptidasesReceptors, Transforming Growth Factor betaRepressor Proteins

Identifiers

PMID29799877
PMCPMC5969754
OpenAlexW2804490133

What OpenQuestion holds

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LicenceCC BY
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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.