Evidence map›Paper›PMID 24741067›Full record

ArticleJournal of cell science2014

Cadherin-11 regulates both mesenchymal stem cell differentiation into smooth muscle cells and the development of contractile function in vivo.

Stella Alimperti, Hui You, Teresa George, Sandeep K Agarwal, Stelios T Andreadis

Abstract read
In one paragraph

Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 80 citations in OpenAlex.

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  12. Effect of Cadherin-11 on the Proliferation, Migration, and ECM Synthesis of Chondrocyte.Journal of tissue engineering and regenerative medicine · 2023
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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.

Stella AlimpertiBioengineering Laboratory, Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Amherst, NY 14260-4200, USA.
Hui YouBioengineering Laboratory, Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Amherst, NY 14260-4200, USA.
Teresa GeorgeBaylor College of Medicine, Department of Medicine, Section of Allergy, Immunology, and Rheumatology, Biology of Inflammation Center, One Baylor Plaza, Suite 672E, MS, BCM285, Houston, TX 77030, USA.
Sandeep K AgarwalBaylor College of Medicine, Department of Medicine, Section of Allergy, Immunology, and Rheumatology, Biology of Inflammation Center, One Baylor Plaza, Suite 672E, MS, BCM285, Houston, TX 77030, USA.
Stelios T AndreadisBioengineering Laboratory, Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Amherst, NY 14260-4200, USA Department of Biomedical Engineering, University at Buffalo, The State University of New York, Amherst, NY 14260-4200, USA Center of Excellence in Bioinformatics and Life Sciences, Buffalo, NY 14203, USA sandread@buffalo.edu.
University at Buffalo, State University of New York · USBaylor College of Medicine · US

Funding

Stem Cells for Vascular Tissue EngineeringR01HL086582 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI ANDREADIS, STELIOS THEOHARIS · 2008 to 2017
$3.1M
NHLBI NIH HHS R01 HL086582
6 · The paper itself

Abstract

Although soluble factors, such as transforming growth factor β1 (TGF-β1), induce mesenchymal stem cell (MSC) differentiation towards the smooth muscle cell (SMC) lineage, the role of adherens junctions in this process is not well understood. In this study, we found that cadherin-11 but not cadherin-2 was necessary for MSC differentiation into SMCs. Cadherin-11 regulated the expression of TGF-β1 and affected SMC differentiation through a pathway that was dependent on TGF-β receptor II (TGFβRII) but independent of SMAD2 or SMAD3. In addition, cadherin-11 activated the expression of serum response factor (SRF) and SMC proteins through the Rho-associated protein kinase (ROCK) pathway. Engagement of cadherin-11 increased its own expression through SRF, indicative of the presence of an autoregulatory feedback loop that committed MSCs to the SMC fate. Notably, SMC-containing tissues (such as aorta and bladder) from cadherin-11-null (Cdh11(-/-)) mice showed significantly reduced levels of SMC proteins and exhibited diminished contractility compared with controls. This is the first report implicating cadherin-11 in SMC differentiation and contractile function in vitro as well as in vivo.

Indexed as

Cell DifferentiationAnimalsCadherinsCell AdhesionCells, CulturedEnzyme ActivationFeedback, PhysiologicalGene ExpressionMesenchymal Stem CellsMice, 129 StrainMice, Inbred C57BLMice, KnockoutMuscle ContractionMuscle DevelopmentMuscle, Smooth, VascularMyocytes, Smooth MuscleCadherinsCdh2 protein, mouseosteoblast cadherinrho-Associated KinasesTgfb1 protein, mouseTransforming Growth Factor beta1Adherens junctionsCell–cell adhesionDifferentiationMesenchymal stem cellsSmooth muscle cellsVascular contractility

Identifiers

PMID24741067
PMCPMC4058109
OpenAlexW2140375804

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.