Evidence map›Paper›PMID 20410440›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010

Sprouty1 is a critical regulatory switch of mesenchymal stem cell lineage allocation.

Sumithra Urs, Deepak Venkatesh, Yuefeng Tang, Terry Henderson, Xuehui Yang, Robert E Friesel, Clifford J Rosen, Lucy Liaw

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

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  11. Unraveling the genotype by environment interaction in a thermosensitive fish with a polygenic sex determination system.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

8 authors at 2 institutions in 1 country.

Sumithra UrsMaine Medical Center Research Institute, 81 Research Dr., Scarborough, ME 04074, USA.
Deepak Venkatesh
Yuefeng Tang
Terry Henderson
Xuehui Yang
Robert E Friesel
Clifford J Rosen
Lucy Liaw
Maine Medical Center Research Institute · USMaine Medical Center · US

Funding

Contribution of Notch Signaling to Vascular RemodelingR01HL070865 · NHLBI · MAINE MEDICAL CENTER · PI LIAW, LUCY · 2003 to 2017
$4.6M
MOUSE MODELS TO DELINEATE A UNIQUE METABOLIC AND SKELETAL NETWORKR01AR054604 · NIAMS · MAINEHEALTH · PI ROSEN, CLIFFORD JAMES · 2007 to 2010
$2.3M
Feedback Inhibitory Mechanisms in Skeletal DevelopmentR01DK073871 · NIDDK · MAINEHEALTH · PI FRIESEL, ROBERT E · 2007 to 2011
$1.7M
DIAGNOSTIC LABORATORY FOR RESEARCH ANIMALSP40RR001555 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI SHALEV, MOSHE · 1985 to 1985
–
NCRR NIH HHS P20RR1555NCRR NIH HHS P20RR181789NHLBI NIH HHS R01 HL070865NHLBI NIH HHS R01HL070865NIAMS NIH HHS AR54604NIAMS NIH HHS R01 AR054604NIDDK NIH HHS DK73871NIDDK NIH HHS R01 DK073871
6 · The paper itself

Abstract

Development of bone and adipose tissue are linked processes arising from a common progenitor cell, but having an inverse relationship in disease conditions such as osteoporosis. Cellular differentiation of both tissues relies on growth factor cues, and we focus this study on Sprouty1 (Spry1), an inhibitor of growth factor signaling. We tested whether Spry1 can modify the development of fat cells through its activity in regulating growth factors known to be important for adipogenesis. We utilized conditional expression and genetic-null mouse models of Spry1 in adipocytes using the fatty acid binding promoter (aP2). Conditional deletion of Spry1 results in 10% increased body fat and decreased bone mass. This phenotype was rescued on Spry1 expression, which results in decreased body fat and increased bone mass. Ex vivo bone marrow experiments indicate Spry1 in bone marrow and adipose progenitor cells favors differentiation of osteoblasts at the expense of adipocytes by suppressing CEBP-beta and PPARgamma while up regulating TAZ. Age and gender-matched littermates expressing only Cre recombinase were used as controls. Spry1 is a critical regulator of adipocyte differentiation and mesenchymal stem cell (MSC) lineage allocation, potentially acting through regulation of CEBP-beta and TAZ.

Indexed as

Cell DifferentiationAbsorptiometry, PhotonAdaptor Proteins, Signal TransducingAdipocytesAdipogenesisAnimalsCCAAT-Enhancer-Binding Protein-betaCells, CulturedHypertrophyImmunoblottingImmunohistochemistryMembrane ProteinsMesenchymal Stem CellsMiceMice, TransgenicNuclear ProteinsAdaptor Proteins, Signal TransducingCCAAT-Enhancer-Binding Protein-betaMembrane ProteinsNuclear ProteinsPhosphoproteinsSpry1 protein, mouseTwist1 protein, mouseTwist-Related Protein 1

Identifiers

PMID20410440
PMCPMC2923355
OpenAlexW2160545539

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.