Evidence map›Paper›PMID 26509098›Full record

ArticleBone research2015

Rho/Rock signal transduction pathway is required for MSC tenogenic differentiation.

Edward Maharam, Miguel Yaport, Nathaniel L Villanueva, Takintope Akinyibi, Damien Laudier, Zhiyong He, Daniel J Leong, Hui B Sun

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 68 citations in OpenAlex.

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  10. Tendon mechanobiology in the context of tendon biofabrication.Frontiers in bioengineering and biotechnology · 2025
    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

8 authors at 2 institutions in 1 country.

Edward MaharamLeni and Peter W. May Department of Orthopedics, Icahn School of Medicine at Mount Sinai , New York, NY, USA.
Miguel YaportLeni and Peter W. May Department of Orthopedics, Icahn School of Medicine at Mount Sinai , New York, NY, USA.
Nathaniel L VillanuevaLeni and Peter W. May Department of Orthopedics, Icahn School of Medicine at Mount Sinai , New York, NY, USA.
Takintope AkinyibiLeni and Peter W. May Department of Orthopedics, Icahn School of Medicine at Mount Sinai , New York, NY, USA.
Damien LaudierLeni and Peter W. May Department of Orthopedics, Icahn School of Medicine at Mount Sinai , New York, NY, USA.
Zhiyong HeDepartments of Orthopedic Surgery, Albert Einstein College of Medicine , Bronx, NY, USA ; Radiation Oncology, Albert Einstein College of Medicine , Bronx, NY, USA.
Daniel J LeongDepartments of Orthopedic Surgery, Albert Einstein College of Medicine , Bronx, NY, USA ; Radiation Oncology, Albert Einstein College of Medicine , Bronx, NY, USA.
Hui B SunDepartments of Orthopedic Surgery, Albert Einstein College of Medicine , Bronx, NY, USA ; Radiation Oncology, Albert Einstein College of Medicine , Bronx, NY, USA.
Icahn School of Medicine at Mount Sinai · USAlbert Einstein College of Medicine · US

Funding

Human tendon stem progenitor cell aging and regenerationR01AG039561 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI FLATOW, EVAN L, SUN, HUI BIN · 2012 to 2016
$2.5M
NIA NIH HHS R01 AG039561
6 · The paper itself

Abstract

Mesenchymal stem cell (MSC)-based treatments have shown promise for improving tendon healing and repair. MSCs have the potential to differentiate into multiple lineages in response to select chemical and physical stimuli, including into tenocytes. Cell elongation and cytoskeletal tension have been shown to be instrumental to the process of MSC differentiation. Previous studies have shown that inhibition of stress fiber formation leads MSCs to default toward an adipogenic lineage, which suggests that stress fibers are required for MSCs to sense the environmental factors that can induce differentiation into tenocytes. As the Rho/ROCK signal transduction pathway plays a critical role in both stress fiber formation and in cell sensation, we examined whether the activation of this pathway was required when inducing MSC tendon differentiation using rope-like silk scaffolds. To accomplish this, we employed a loss-of-function approach by knocking out ROCK, actin and myosin (two other components of the pathway) using the specific inhibitors Y-27632, Latrunculin A and blebbistatin, respectively. We demonstrated that independently disrupting the cytoskeleton and the Rho/ROCK pathway abolished the expression of tendon differentiation markers and led to a loss of spindle morphology. Together, these studies suggest that the tension that is generated by MSC elongation is essential for MSC teno-differentiation and that the Rho/ROCK pathway is a critical mediator of tendon differentiation on rope-like silk scaffolds.

Identifiers

PMID26509098
PMCPMC4605238
OpenAlexW1956262082

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.