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1 Anatomy, Histology, Forensic Medicine, University of Florence, Florence, Italy
2 Physiological Science, University of Florence, Florence, Italy
3 Experimental Surgery Unit, Careggi Hospital, Florence, Italy
* To whom correspondence should be addressed. E-mail: formigli{at}unifi.it.
The success of cellular cardiomyoplasty, a novel therapy for the repair of post-ischemic myocardium, depends on the anatomical integration of the engrafted cells with the resident cardiomyocytes. Our aim was to investigate the interaction between undifferentiated mouse skeletal myoblasts (C2C12 cells) and adult rat ventricular cardiomyocytes in an in vitro model of coculture. Connexin 43 (Cx43) expression, Lucifer yellow microinjection, calcium transient propagation, and electrophysiological analysis demonstrated that myoblasts and cardiomyocytes were coupled by functional gap junctions. We also showed that cardiomyocytes upregulated gap junctional communication and expression of Cx43 in myoblasts. This effect required direct cell-to-cell contact between the two cell types and was potentiated by treatment with relaxin, a cardiotropic hormone with potential effects on cardiac development. Analysis of the gating properties of gap junctions by dual cell patch clamp showed that the co-presence of cardiomyocytes in the cultures significantly increased the transjunctional current and conductance between myoblasts. Relaxin enhanced this effect in both the myoblast-myoblast and myoblast-cardiomyocyte cell pairs, likely acting not only on gap junction formation, but also on the electrical properties of the pre-existing channels. In conclusion, our findings suggest that myoblasts and cardiomyocytes interact actively through gap junctions and that relaxin potentiates the intercellular coupling. A potential role for gap junctional communication in favoring the intercellular exchange of regulatory molecules, including Ca2+, in the modulation of myoblast differentiation is discussed.
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