Evidence map›Paper›PMID 25409310›Full record

ArticlePloS one2014

Development of an OP9 derived cell line as a robust model to rapidly study adipocyte differentiation.

Jacqueline M Lane, Jamie R Doyle, Jean-Philippe Fortin, Alan S Kopin, José M Ordovás

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 33% 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

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

  1. Pooled it
  2. Review
  3. A Review onEndocrine, metabolic & immune disorders drug targets · 2025
    Review
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  5. Antiobesity Drug Discovery Research:Current drug targets · 2024
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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 at 2 institutions in 1 country.

Jacqueline M LaneMassachusetts General Hospital, Center for Human Genetics Research, 185 Cambridge Street, Boston, MA 02114, United States of America; Division of Sleep Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, United States of America; Jean Mayer-USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, United States of America.
Jamie R DoyleTufts Medical Center, Molecular Cardiology Research Institute, Molecular Pharmacology Research Center, 800 Washington St., Box 7703, Boston, MA 02111, United States of America.
Jean-Philippe FortinTufts Medical Center, Molecular Cardiology Research Institute, Molecular Pharmacology Research Center, 800 Washington St., Box 7703, Boston, MA 02111, United States of America.
Alan S KopinTufts Medical Center, Molecular Cardiology Research Institute, Molecular Pharmacology Research Center, 800 Washington St., Box 7703, Boston, MA 02111, United States of America.
José M OrdovásJean Mayer-USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, United States of America.
Tufts Medical Center · USTufts University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One hallmark of obesity is adipocyte hypertrophy and hyperplasia. To gain novel insights into adipose biology and therapeutics, there is a pressing need for a robust, rapid, and informative cell model of adipocyte differentiation for potential RNAi and drug screens. Current models are prohibitive for drug and RNAi screens due to a slow differentiation time course and resistance to transfection. We asked if we could create a rapid, robust model of adipogenesis to potentially enable rapid functional and obesity therapeutic screens. We generated the clonal population OP9-K, which differentiates rapidly and reproducibly, and displays classic adipocyte morphology: rounded cell shape, lipid accumulation, and coalescence of lipids into a large droplet. We further validate the OP9-K cells as an adipocyte model system by microarray analysis of the differentiating transcriptome. OP9-K differentiates via known adipogenic pathways, involving the transcriptional activation and repression of common adipose markers Plin1, Gata2, C/Ebpα and C/Ebpβ and biological pathways, such as lipid metabolism, PPARγ signaling, and osteogenesis. We implemented a method to quantify lipid accumulation using automated microscopy and tested the ability of our model to detect alterations in lipid accumulation by reducing levels of the known master adipogenic regulator Pparγ. We further utilized our model to query the effects of a novel obesity therapeutic target, the transcription factor SPI1. We determine that reduction in levels of Spi1 leads to an increase in lipid accumulation. We demonstrate rapid, robust differentiation and efficient transfectability of the OP9-K cell model of adipogenesis. Together with our microscopy based lipid accumulation assay, adipogenesis assays can be achieved in just four days' time. The results of this study can contribute to the development of rapid screens with the potential to deepen our understanding of adipose biology and efficiently test obesity therapeutics.

Indexed as

AdipogenesisModels, BiologicalAdipocytesAnimalsCell LineLipid MetabolismMiceProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID25409310
PMCPMC4237323
OpenAlexW2024105065

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.