Cargando…

Microcurrent stimulation promotes reverse remodelling in cardiomyocytes

AIMS: It has been shown that electrical stimulation can improve tissue repair in patients. Imbalances in the extracellular matrix composition induce manifestation of heart failure. Here we investigated the application of microcurrent (MC) to modulate the expression of matrix metalloproteinases (MMPs...

Descripción completa

Detalles Bibliográficos
Autores principales: Kapeller, Barbara, Mueller, Johannes, Losert, Udo, Podesser, Bruno K., Macfelda, Karin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064659/
https://www.ncbi.nlm.nih.gov/pubmed/27774272
http://dx.doi.org/10.1002/ehf2.12080
_version_ 1782460202797236224
author Kapeller, Barbara
Mueller, Johannes
Losert, Udo
Podesser, Bruno K.
Macfelda, Karin
author_facet Kapeller, Barbara
Mueller, Johannes
Losert, Udo
Podesser, Bruno K.
Macfelda, Karin
author_sort Kapeller, Barbara
collection PubMed
description AIMS: It has been shown that electrical stimulation can improve tissue repair in patients. Imbalances in the extracellular matrix composition induce manifestation of heart failure. Here we investigated the application of microcurrent (MC) to modulate the expression of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) in cardiomyocytes in vitro and in vivo to reverse remodelling in the heart in spontaneous hypertensive rats (SHR). METHODS: Cardiomyocytes from young SHR (7 months) and old SHR (14 months) were stimulated in vitro and in vivo with MC. MMP and TIMP expression were analysed by qPCR and immunofluorescence to evaluate the modulation of MC treatment. RESULTS: Modulation of cardiomyocytes with MC enhances proliferation with no morphological changes in vitro. By electrical stimulation dual effects, increase and decrease, on MMP‐2, MMP‐9, TIMP‐3, and TIMP‐4 mRNA as well as protein expression were observed, depending on the age of the cardiomyocytes. In our in vivo study, MC down‐regulated MMP‐2, MMP‐9, and TIMP‐4 and increased TIMP‐3 in young SHR. In old SHR MMP‐2, MMP‐9, and TIMP‐4 were up‐regulated, whereas TIMP‐3 was unaffected. CONCLUSIONS: Our data indicate that treatment of MC can modulate the expression of MMPs and TIMPs in vitro and in vivo in SHR. Based on these results new treatments for heart failure could be developed.
format Online
Article
Text
id pubmed-5064659
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-50646592016-10-19 Microcurrent stimulation promotes reverse remodelling in cardiomyocytes Kapeller, Barbara Mueller, Johannes Losert, Udo Podesser, Bruno K. Macfelda, Karin ESC Heart Fail Original Research Articles AIMS: It has been shown that electrical stimulation can improve tissue repair in patients. Imbalances in the extracellular matrix composition induce manifestation of heart failure. Here we investigated the application of microcurrent (MC) to modulate the expression of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) in cardiomyocytes in vitro and in vivo to reverse remodelling in the heart in spontaneous hypertensive rats (SHR). METHODS: Cardiomyocytes from young SHR (7 months) and old SHR (14 months) were stimulated in vitro and in vivo with MC. MMP and TIMP expression were analysed by qPCR and immunofluorescence to evaluate the modulation of MC treatment. RESULTS: Modulation of cardiomyocytes with MC enhances proliferation with no morphological changes in vitro. By electrical stimulation dual effects, increase and decrease, on MMP‐2, MMP‐9, TIMP‐3, and TIMP‐4 mRNA as well as protein expression were observed, depending on the age of the cardiomyocytes. In our in vivo study, MC down‐regulated MMP‐2, MMP‐9, and TIMP‐4 and increased TIMP‐3 in young SHR. In old SHR MMP‐2, MMP‐9, and TIMP‐4 were up‐regulated, whereas TIMP‐3 was unaffected. CONCLUSIONS: Our data indicate that treatment of MC can modulate the expression of MMPs and TIMPs in vitro and in vivo in SHR. Based on these results new treatments for heart failure could be developed. John Wiley and Sons Inc. 2016-01-06 /pmc/articles/PMC5064659/ /pubmed/27774272 http://dx.doi.org/10.1002/ehf2.12080 Text en © 2016 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Research Articles
Kapeller, Barbara
Mueller, Johannes
Losert, Udo
Podesser, Bruno K.
Macfelda, Karin
Microcurrent stimulation promotes reverse remodelling in cardiomyocytes
title Microcurrent stimulation promotes reverse remodelling in cardiomyocytes
title_full Microcurrent stimulation promotes reverse remodelling in cardiomyocytes
title_fullStr Microcurrent stimulation promotes reverse remodelling in cardiomyocytes
title_full_unstemmed Microcurrent stimulation promotes reverse remodelling in cardiomyocytes
title_short Microcurrent stimulation promotes reverse remodelling in cardiomyocytes
title_sort microcurrent stimulation promotes reverse remodelling in cardiomyocytes
topic Original Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064659/
https://www.ncbi.nlm.nih.gov/pubmed/27774272
http://dx.doi.org/10.1002/ehf2.12080
work_keys_str_mv AT kapellerbarbara microcurrentstimulationpromotesreverseremodellingincardiomyocytes
AT muellerjohannes microcurrentstimulationpromotesreverseremodellingincardiomyocytes
AT losertudo microcurrentstimulationpromotesreverseremodellingincardiomyocytes
AT podesserbrunok microcurrentstimulationpromotesreverseremodellingincardiomyocytes
AT macfeldakarin microcurrentstimulationpromotesreverseremodellingincardiomyocytes