Abstract
Heart disease is the number one killer in the USA. The collective contractility of the muscle cells of the myocardium - cardiomyocytes - generates the necessary force for the function of a healthy beating heart. Laminin interacts in vivo with cardiomyocytes. Changes in the extracellular concentration and organization of laminin relate to different types of heart disease. Arrays of polydimethylsiloxane (PDMS) microposts measure forces generated by adhesive mammalian cells and were here used to characterize the contractility of single neonatal cardiomyocytes. We used two types of organosilanes to bind laminin to the surface of PDMS microposts: 3-glycidoxypropyltrimethoxysilane and 3-aminopropyltriethoxysilane. We acquired videos of contracting cardiomyocytes at two different days after cells started to beat and functionally characterized the contractility of single cells. More specifically, we calculated generated forces, beating rate, time of contractions and speeds of contraction and relaxation. These parameters varied in time as a function of organosilane surface stability and cardiomyocyte biological changes when cultured in vitro. Higher forces are generated by cardiomyocytes cultured on laminin covalently attached to PDMS microposts relative to laminin physisorbed to oxidized PDMS. We obtained higher laminin density with 3-glycidoxypropyltrimethoxysilane, which correlated to higher generated forces. We also observed higher beating rate at the day 1 and a considerable decrease at day 2. Compared to 3-glycidoxypropyltrimethoxysilane, higher stability of laminin covalent attachment was observed with 3-aminopropyltriethoxysilane. The beating rate and speeds of contraction and relaxation increased and time of contractions decreased at day 2 for neonatal cardiomyocytes cultured on these PDMS micropost surfaces. Our results shed light on the potential of in vitro biomechanical systems to model extracellular disease conditions of heart pathologies. Future work will test the contractility of cardiomyocytes with mutations known to originate cardiomyopathies.
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