Abstract
Myocardial infarction is one of the largest contributors to cardiovascular disease and reduces the ability of the heart to pump blood. One promising therapeutic approach to address the diminished function is the use of cardiac patches composed of biomaterial substrates and cardiac cells. These patches can be enhanced with the application of an auxetic design, which has a negative Poisson’s ratio and can be modified to suit the mechanics of the infarct and surrounding cardiac tissue. Here, we examined multiple auxetic models (orthogonal missing rib and re-entrant honeycomb in two orientations) with tunable mechanical properties as a cardiac patch substrate. Further, we demonstrated that 3D printing based auxetic cardiac patches of varying thicknesses (0.2, 0.4, and 0.6 mm) composed of polycaprolactone and gelatin methacrylate can support induced pluripotent stem cell-derived cardiomyocyte function for 14-day culture. Taken together, this work shows the potential of cellularized auxetic cardiac patches as a suitable tissue engineering approach to treating cardiovascular disease.
Highlights
Myocardial infarction (MI) is a leading contributor to worldwide morbidity and mortality, which is associated with weakening of the left ventricle, leading to heart failure [1]
We further demonstrated that a 3D printing based auxetic cardiac patch composed of auxetic polycaprolactone (PCL) substrate and gelatin methacrylate (GelMA) is capable of supporting human induced pluripotent stem cell-derived cardiomyocytes as a potential therapy
We were able to create an auxetic patch composed of PCL, a biocompatible thermoplastic polymer that has been approved by the US Food and Drug Administration (FDA) for clinical use (K123633 FDA 510 k approval), and GelMA, which we showed maintains iPSC-CM phenotype and function at both a high and low cell density
Summary
Myocardial infarction (MI) is a leading contributor to worldwide morbidity and mortality, which is associated with weakening of the left ventricle, leading to heart failure [1]. Following MI, the ventricular walls undergo intensive remodeling of the infarcted area, resulting in thinning, fibrosis, and reduced cardiac output [2,3,4]. This process alters the heart microenvironment, which cannot be reversed by generation of new contractile tissue [2,3,4,5]. These changes elicit major consequences on the geometry and function of the heart, often causing permanent adverse remodeling. Progression to the clinic has been limited by poor engraftment associated with cell therapies, as well as inappropriate biological cues [6,7,8]
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