Evidence map›Paper›PMID 26154752›Full record

ArticleTissue engineering. Part A2015

A Tissue-Engineered Chondrocyte Cell Sheet Induces Extracellular Matrix Modification to Enhance Ventricular Biomechanics and Attenuate Myocardial Stiffness in Ischemic Cardiomyopathy.

Yasuhiro Shudo, Jeffrey E Cohen, John W MacArthur, Andrew B Goldstone, Satoru Otsuru, Alen Trubelja, Jay Patel, Bryan B Edwards, George Hung, Alexander S Fairman and 7 more

Abstract read
In one paragraph

Article in Tissue engineering. Part A, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 12 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

17 authors at 3 institutions in 2 countries.

Yasuhiro Shudo1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
Jeffrey E Cohen1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
John W MacArthur1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
Andrew B Goldstone1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
Satoru Otsuru3 Center for Childhood Cancer and Blood Diseases, The Research Institute , Nationwide Children's Hospital, Columbus, Ohio.
Alen Trubelja2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
Jay Patel1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
Bryan B Edwards1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
George Hung2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
Alexander S Fairman2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
Christopher Brusalis2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
William Hiesinger2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
Pavan Atluri2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
Arudo Hiraoka2 Division of Cardiovascular Surgery, Department of Surgery, University of Pennsylvania School of Medicine , Philadelphia, Pennsylvania.
Shigeru Miyagawa4 Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine , Osaka, Japan .
Yoshiki Sawa4 Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine , Osaka, Japan .
Y Joseph Woo1 Department of Cardiothoracic Surgery, Stanford University School of Medicine , Stanford, California.
University of Pennsylvania · USStanford University · USOsaka University · JP

Funding

ANGIOGENIC TISSUE ENGINEERING TO LIMIT POST-INFARCTION VENTRICULAR REMODELINGR01HL089315 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI WOO, Y JOSEPH · 2008 to 2023
$6.4M
NHLBI NIH HHS 1R01HL089315-01NHLBI NIH HHS R01 HL089315
6 · The paper itself

Abstract

There exists a substantial body of work describing cardiac support devices to mechanically support the left ventricle (LV); however, these devices lack biological effects. To remedy this, we implemented a cell sheet engineering approach utilizing chondrocytes, which in their natural environment produce a relatively elastic extracellular matrix (ECM) for a cushioning effect. Therefore, we hypothesized that a chondrocyte cell sheet applied to infarcted and borderzone myocardium will biologically enhance the ventricular ECM and increase elasticity to augment cardiac function in a model of ischemic cardiomyopathy (ICM). Primary articular cartilage chondrocytes of Wistar rats were isolated and cultured on temperature-responsive culture dishes to generate cell sheets. A rodent ICM model was created by ligating the left anterior descending coronary artery. Rats were divided into two groups: cell sheet transplantation (1.0 × 10(7) cells/dish) and no treatment. The cell sheet was placed onto the surface of the heart covering the infarct and borderzone areas. At 4 weeks following treatment, the decreased fibrotic extension and increased elastic microfiber networks in the infarct and borderzone areas correlated with this technology's potential to stimulate ECM formation. The enhanced ventricular elasticity was further confirmed by the axial stretch test, which revealed that the cell sheet tended to attenuate tensile modulus, a parameter of stiffness. This translated to increased wall thickness in the infarct area, decreased LV volume, wall stress, mass, and improvement of LV function. Thus, the chondrocyte cell sheet strengthens the ventricular biomechanical properties by inducing the formation of elastic microfiber networks in ICM, resulting in attenuated myocardial stiffness and improved myocardial function.

Indexed as

AnimalsBlotting, WesternCardiomyopathiesChondrocytesImmunohistochemistryMaleRatsRats, WistarTissue Engineering

Identifiers

PMID26154752
PMCPMC4605354
OpenAlexW1961338138

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.