Evidence map›Paper›PMID 26956209›Full record

ArticleStem cells translational medicine2016

Enhanced Osteogenesis of Adipose-Derived Stem Cells by Regulating Bone Morphogenetic Protein Signaling Antagonists and Agonists.

Jiabing Fan, Choong Sung Im, Mian Guo, Zhong-Kai Cui, Armita Fartash, Soyon Kim, Nikhil Patel, Olga Bezouglaia, Benjamin M Wu, Cun-Yu Wang and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

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  8. Bioactive materials forBioactive materials · 2024
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  18. A Review of Recent Developments in the Molecular Mechanisms of Bone Healing.International journal of molecular sciences · 2021
    Review
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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

12 authors at 2 institutions in 2 countries.

Jiabing FanDivision of Advanced Prosthodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Choong Sung ImDivision of Advanced Prosthodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Mian GuoDepartment of Neurosurgery, 2nd Affiliated Hospital of Harbin Medical University, Harbin, Heilonjiang, People's Republic of China.
Zhong-Kai CuiDivision of Advanced Prosthodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Armita FartashDivision of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, Los Angeles, California, USA.
Soyon KimDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Nikhil PatelDivision of Advanced Prosthodontics, School of Dentistry, University of California, Los Angeles, California, USA.
Olga BezouglaiaDivision of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, Los Angeles, California, USA.
Benjamin M WuDivision of Advanced Prosthodontics, School of Dentistry, University of California, Los Angeles, California, USA Department of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Cun-Yu WangDivision of Oral Biology and Medicine, School of Dentistry, University of California, Los Angeles, Los Angeles, California, USA.
Tara L AghalooDivision of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, Los Angeles, California, USA leemin@ucla.edu taghaloo@dentistry.ucla.edu.
Min LeeDivision of Advanced Prosthodontics, School of Dentistry, University of California, Los Angeles, California, USA Department of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA leemin@ucla.edu taghaloo@dentistry.ucla.edu.
University of California, Los Angeles · USHarbin Medical University · CN

Funding

Molecular Regulation of Human Dental Stem Cell PropertyR01DE016513 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2005 to 2019
$6.0M
Combined Effect of Noggin Suppression and Nell-1 on Bone RegenerationR01AR060213 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEE, MIN · 2011 to 2015
$1.7M
Molecular Control of MSC differentiation and Bone Formation by KDM4BR01AR063089 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, CUN-YU · 2013 to 2017
$1.6M
Biomimetic Scaffold Delivering Osteogenic Molecules for Alveolar Bone EngineeringR21DE021819 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEE, MIN · 2012 to 2013
$416k
NIAMS NIH HHS R01 AR060213NIAMS NIH HHS R01 AR063089NIDCR NIH HHS R01 DE016513NIDCR NIH HHS R21 DE021819
6 · The paper itself

Abstract

unlabelledAlthough adipose-derived stem cells (ASCs) are an attractive cell source for bone tissue engineering, direct use of ASCs alone has had limited success in the treatment of large bone defects. Although bone morphogenetic proteins (BMPs) are believed to be the most potent osteoinductive factors to promote osteogenic differentiation of ASCs, their clinical applications require supraphysiological dosage, leading to high medical burden and adverse side effects. In the present study, we demonstrated an alternative approach that can effectively complement the BMP activity to maximize the osteogenesis of ASCs without exogenous application of BMPs by regulating levels of antagonists and agonists to BMP signaling. Treatment of ASCs with the amiloride derivative phenamil, a positive regulator of BMP signaling, combined with gene manipulation to suppress the BMP antagonist noggin, significantly enhanced osteogenic differentiation of ASCs through increased BMP-Smad signaling in vitro. Furthermore, the combination approach of noggin suppression and phenamil stimulation enhanced the BMP signaling and bone repair in a mouse calvarial defect model by adding noggin knockdown ASCs to apatite-coated poly(lactic-coglycolic acid) scaffolds loaded with phenamil. These results suggest novel complementary osteoinductive strategies that could maximize activity of the BMP pathway in ASC bone repair while reducing potential adverse effects of current BMP-based therapeutics. SIGNIFICANCE: Although stem cell-based tissue engineering strategy offers a promising alternative to repair damaged bone, direct use of stem cells alone is not adequate for challenging healing environments such as in large bone defects. This study demonstrates a novel strategy to maximize bone formation pathways in osteogenic differentiation of mesenchymal stem cells and functional bone formation by combining gene manipulation with a small molecule activator toward osteogenesis. The findings indicate promising stem cell-based therapy for treating bone defects that can effectively complement or replace current osteoinductive therapeutics.

Indexed as

Adipose TissueAdult Stem CellsAmilorideAnimalsBone Morphogenetic ProteinsCarrier ProteinsCell DifferentiationCells, CulturedMaleMiceMice, Inbred C57BLMice, NudeNoggin ProteinOsteogenesisSignal TransductionSmad ProteinsAmilorideBone Morphogenetic ProteinsCarrier ProteinsNoggin ProteinphenylamilSmad ProteinsAdipose-derived stem cellsBMP–Smad signalingNogginOsteogenesisPhenamil

Identifiers

PMID26956209
PMCPMC4798741
OpenAlexW2293852376

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.