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(Circulation Research. 2008;103:340.)
© 2008 American Heart Association, Inc.

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Myofibrillar Architecture in Engineered Cardiac Myocytes

Kevin Kit Parker, John Tan, Christopher S. Chen, Leslie Tung

From the Disease Biophysics Group (K.K.P.), School of Engineering and Applied Sciences, Harvard University, Cambridge, Mass; California Institute of Technology (J.T.), Pasadena; Department of Bioengineering (C.S.C.), University of Pennsylvania, Philadelphia; and Department of Biomedical Engineering (L.T.), The Johns Hopkins University, Baltimore, Md.

Correspondence to Kevin Kit Parker, Disease Biophysics Group, School of Engineering and Applied Sciences, Harvard University, 29 Oxford St, Pierce Hall 321, Cambridge, MA 02138. E-mail kkparker@ seas.harvard.edu

Morphogenesis is often considered a function of transcriptional synchrony and the spatial limits of diffusing mitogens; however, physical constrainment by the cell microenvironment represents an additional mechanism for regulating self-assembly of subcellular structures. We asked whether myocyte shape is a distinct signal that potentiates the organization of myofibrillar arrays in cardiac muscle myocytes. We engineered the shape of neonatal rat ventricular myocytes by culturing them on microfabricated fibronectin islands, where they spread and assumed the shape of the island. Myofibrillogenesis followed, both spatially and temporally, the assembly of unique actin networks whose architecture was predictable given the shape of the island. Subsequently, the z lines of the sarcomeres aligned and registered in distinct patterns in different regions of the myocytes in such a way that orthogonal axes of contraction could be distinctly engineered. These data suggest that physical constrainment of muscle cells by extracellular matrix may be an important regulator of myofibrillar organization.

Key Words: cardiac myocyte • myofibril • sarcomere • cytoskeleton

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