Evidence map›Paper›PMID 26045895›Full record

ArticleAmerican journal of translational research2015

In vitro comparative study of two decellularization protocols in search of an optimal myocardial scaffold for recellularization.

Isaac Perea-Gil, Juan J Uriarte, Cristina Prat-Vidal, Carolina Gálvez-Montón, Santiago Roura, Aida Llucià-Valldeperas, Carolina Soler-Botija, Ramon Farré, Daniel Navajas, Antoni Bayes-Genis

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  10. ECM roles and biomechanics in cardiac tissue decellularization.American journal of physiology. Heart and circulatory physiology · 2022
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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

10 authors at 1 institution in 1 country.

Isaac Perea-GilICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain.
Juan J UriarteBiophysics and Bioengineering Unit, Faculty of Medicine, University of Barcelona Barcelona, Spain ; CIBER Enfermedades Respiratorias Madrid, Spain.
Cristina Prat-VidalICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain.
Carolina Gálvez-MontónICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain.
Santiago RouraICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain.
Aida Llucià-ValldeperasICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain.
Carolina Soler-BotijaICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain.
Ramon FarréBiophysics and Bioengineering Unit, Faculty of Medicine, University of Barcelona Barcelona, Spain ; CIBER Enfermedades Respiratorias Madrid, Spain ; Institut d'Investigacions Biomèdiques August Pi i Sunyer Barcelona, Spain.
Daniel NavajasBiophysics and Bioengineering Unit, Faculty of Medicine, University of Barcelona Barcelona, Spain ; CIBER Enfermedades Respiratorias Madrid, Spain ; Institute for Bioengineering of Catalonia Barcelona, Spain.
Antoni Bayes-GenisICREC (Heart Failure and Cardiac Regeneration) Research Lab, Health Sciences Research Institute Germans Trias i Pujol (IGTP). Cardiology Service, Hospital Universitari Germans Trias i Pujol Badalona, Barcelona, Spain ; Department of Medicine, Autonomous University of Barcelona (UAB) Barcelona, Spain.
Universitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSelection of a biomaterial-based scaffold that mimics native myocardial extracellular matrix (ECM) architecture can facilitate functional cell attachment and differentiation. Although decellularized myocardial ECM accomplishes these premises, decellularization processes may variably distort or degrade ECM structure. MATERIALS AND

methodsTwo decellularization protocols (DP) were tested on porcine heart samples (epicardium, mid myocardium and endocardium). One protocol, DP1, was detergent-based (SDS and Triton X-100), followed by DNase I treatment. The other protocol, DP2, was focused in trypsin and acid with Triton X-100 treatments. Decellularized myocardial scaffolds were reseeded by embedding them in RAD16-I peptidic hydrogel with adipose tissue-derived progenitor cells (ATDPCs).

resultsBoth protocols yielded acellular myocardial scaffolds (~82% and ~94% DNA reduction for DP1 and DP2, respectively). Ultramicroscopic assessment of scaffolds was similar for both protocols and showed filamentous ECM with preserved fiber disposition and structure. DP1 resulted in more biodegradable scaffolds (P = 0.04). Atomic force microscopy revealed no substantial ECM stiffness changes post-decellularization compared to native tissue. The Young's modulus did not differ between heart layers (P = 0.69) or decellularization protocols (P = 0.15). After one week, recellularized DP1 scaffolds contained higher cell density (236 ± 106 and 98 ± 56 cells/mm(2) for recellularized DP1 and DP2 scaffolds, respectively; P = 0.04). ATDPCs in both DP1 and DP2 scaffolds expressed the endothelial marker isolectin B4, but only in the DP1 scaffold ATDPCs expressed the cardiac markers GATA4, connexin43 and cardiac troponin T.

conclusionsIn our hands, DP1 produced myocardial scaffolds with higher cell repopulation and promotes ATDPCs expression of endothelial and cardiomyogenic markers.

Indexed as

acellular myocardial scaffoldadipose tissue-derived progenitor cellsdecellularization protocolsextracellular matrixMyocardial infarctionrecellularization

Identifiers

PMID26045895
PMCPMC4448195
OpenAlexW2416391489

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.