Recombinant human collagen-based microspheres mitigate cardiac conduction slowing induced by adipose tissue-derived stromal cells

Nicoline W. Smit*, Judith N. ten Sande, Mojtaba Parvizi, Shirley C. M. van Amersfoorth, Josee A. Plantinga, Carolien A. F. M. van Spreuwel-Goossens, Elisabeth M. W. M. van Dongen, Pascal F. H. M. van Dessel, Sebastianus G. J. M. Kluijtmans, Veronique M. F. Meijborg, Jacques M. T. de Bakker, Martin C. Harmsen, Ruben Coronel

*Bijbehorende auteur voor dit werk

OnderzoeksoutputAcademicpeer review

8 Citaten (Scopus)
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Stem cell therapy to improve cardiac function after myocardial infarction is hampered by poor cell retention, while it may also increase the risk of arrhythmias by providing an arrhythmogenic substrate. We previously showed that porcine adipose tissue-derived-stromal cells (pASC) induce conduction slowing through paracrine actions, whereas rat ASC (rASC) and human ASC (hASC) induce conduction slowing by direct coupling. We postulate that biomaterial microspheres mitigate the conduction slowing influence of pASC by interacting with paracrine signaling.


To investigate the modulation of ASC-loaded recombinant human collagen-based microspheres, on the electrophysiological behavior of neonatal rat ventricular myocytes (NRVM).


Unipolar extracellular electrograms, derived from microelectrode arrays (8x8 electrodes) containing NRVM, co-cultured with ASC or ASC loaded microspheres, were used to determine conduction velocity (CV) and conduction heterogeneity. Conditioned medium (Cme) of (co)cultures was used to assess paracrine mechanisms.


Microspheres did not affect CV in control (NRVM) monolayers. In co-cultures of NRVM and rASC, hASC or pASC, CV was lower than in controls (14.4+/-1.0, 13.0+/-0.6 and 9.0+/-1.0 vs. 19.5+/-0.5 cm/s respectively, p


The application of recombinant human collagen-based microspheres mitigates indirect paracrine conduction slowing through interference with a secondary autocrine myocardial factor.

Originele taal-2English
Aantal pagina's20
TijdschriftPLoS ONE
Nummer van het tijdschrift8
StatusPublished - 24-aug-2017

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