alexa OSM-Stimulated Cardiomyocytes Release a C-Terminal Fragment of FGF23
ISSN: 2157-7013

Journal of Cell Science & Therapy
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Research Article

OSM-Stimulated Cardiomyocytes Release a C-Terminal Fragment of FGF23

Ranganath Maringanti1, Thomas Kubin1, Ayse Cetinkaya1, Markus Schönburg1, Andres Beiras-Fernandez3, Thomas Braun2, Thomas Walther1, Sawa Kostin2 and Manfred Richter1*

1Department of Cardiac Surgery, Kerckhoff-Clinic, Benekestrasse, Bad Nauheim, Germany

2Department of Heart and Lung Research, Max-Planck-Institute, Bad Nauheim, Germany

3Department of Cardiothoracic and Vascular Surgery, University Medical Center, Mainz, Mainz, Germany

*Corresponding Author:
Manfred Richter
Department of Cardiac Surgery
Kerckhoff-Clinic, Benekestrasse 2-8
Bad Nauheim, Germany
Tel: +496032996-2774
E-mail: [email protected]

Received Date: May 17, 2017 Accepted Date: June 12, 2017 Published Date: June 14, 2017

Citation: Maringanti R, Kubin T, Cetinkaya A, Schönburg M, Fernandez AB, etal. (2017) OSM-Stimulated Cardiomyocytes Release a C-Terminal Fragment of FGF23. J Cell Sci Ther 8: 273. doi:10.4172/2157-7013. 1000273

Copyright: © 2017 Maringanti R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited



Background: Recent studies emphasize a correlation of increased FGF23 with the pathogenesis of heart diseases. Although it is widely assumed that the bone and not the heart is the major source of FGF23 we previously demonstrated that oncostatin M (OSM) activated cardiomyocytes strongly secrete FGF23. This phosphatonin can be released as intact molecule (iFGF23) as well as C-terminal (cFGF23) and N-terminal (nFGF23) fragments. Since cleavage does not only inactivate iFGF23 but might also exert antagonizing activity we wanted to determine which form is secreted by cardiomyocytes.

Methods: Adult cultured cardiomyocytes were stimulated with OSM or albumin as control. Supernatant and cell lysate were analyzed by Western blot (WB) and specific ELISAs against cFGF23 as well as iFGF23. Expression of FGF23 in cardiomyocytes of 6 patients with coronary heart diseases (CHD) was analyzed by confocal microscopy because OSM signaling cascades are activated after myocardial infarction.

Results: WB analysis identified cFGF23 as well as nFGF23 while iFGF23 was hardly detectable in the supernatant of OSM-stimulated cardiomyocytes. Analysis of the supernatant by ELISAs revealed that less than 3% of this secreted phosphatonin was intact. In patients with CHD the number of FGF23 positive cardiomyocytes increased from 0.2% in the remote zone to 4.4% in the border zone.

Conclusions: The expression and release of FGF23 by cardiomyocytes indicate local as well as systemic functions. The determination of the ratio of iFGF23/cFGF23 will be essential to understand the functional role of this growth factor in patients with cardiac diseases.


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