Evidence map›Paper›PMID 26340021›Full record

ArticlePloS one2015

AFAP1 Is a Novel Downstream Mediator of TGF-β1 for CCN2 Induction in Osteoblasts.

Youngjin Cho, Rachel Silverstein, Max T Geisinger, Stephen Martinkovich, Holly Corkill, Jess M Cunnick, Sonia L Planey, John A Arnott

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 11 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

8 authors at 1 institution in 1 country.

Youngjin ChoThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Rachel SilversteinThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Max T GeisingerThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Stephen MartinkovichThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Holly CorkillThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Jess M CunnickThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Sonia L PlaneyThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
John A ArnottThe Commonwealth Medical College, Scranton, Pennslyvania, United States of America.
Commonwealth Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCCN2 acts as an anabolic growth factor to regulate osteoblast differentiation and function. CCN2 is induced by TGF-β1 and acts as a mediator of TGF-β1 induced matrix production in osteoblasts and Src is required for CCN2 induction by TGF-β1; however, the molecular mechanisms that control CCN2 induction in osteoblasts are poorly understood. AFAP1 binds activated forms of Src and can direct the activation of Src in certain cell types, however a role for AFAP1 downstream of TGF-β1 or in osteoblats is undefined. In this study, we investigated the role of AFAP1 for CCN2 induction by TGF-β1 in primary osteoblasts.

resultsWe demonstrated that AFAP1 expression in osteoblasts occurs in a biphasic pattern with maximal expression levels occurring during osteoblast proliferation (~day 3), reduced expression during matrix production/maturation (~day 14-21), an a further increase in expression during mineralization (~day 21). AFAP1 expression is induced by TGF-β1 treatment in osteoblasts during days 7, 14 and 21. In osteoblasts, AFAP1 binds to Src and is required for Src activation by TGF-β1 and CCN2 promoter activity and protein induction by TGF-β1 treatment was impaired using AFAP1 siRNA, indicating the requirement of AFAP1 for CCN2 induction by TGF-β1. We also demonstrated that TGF-β1 induction of extracellular matrix protein collagen XIIa occurs in an AFAP1 dependent fashion.

conclusionsThis study demonstrates that AFAP1 is an essential downstream signaling component of TGF-β1 for Src activation, CCN2 induction and collagen XIIa in osteoblasts.

Indexed as

AnimalsAnimals, NewbornBinding SitesCell DifferentiationCell ProliferationCollagen Type XIIConnective Tissue Growth FactorGene Expression RegulationMicrofilament ProteinsOsteoblastsPrimary Cell CulturePromoter Regions, GeneticProtein BindingProto-Oncogene Proteins pp60(c-src)RatsRats, Sprague-DawleyAfap1 protein, ratCCN2 protein, ratCollagen Type XIIConnective Tissue Growth FactorMicrofilament ProteinsProto-Oncogene Proteins pp60(c-src)RNA, Small InterferingTransforming Growth Factor beta1

Identifiers

PMID26340021
PMCPMC4560384
OpenAlexW2172707085

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LicenceCC BY
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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.