AUTHORS:

J. C. Dallon 1 and H. Paul Ehrlich 2

1: Department of Mathematics, Brigham Young University, Provo, UT 84602-6539

2: Division of Plastic Surgery, Department of Surgery, Milton S. Hershey Medical Center, Hershey, PA

ABSTRACT:

This cell populated collagen lattice (PCL) study compares lattice contraction by myofibroblasts and blood vessel smooth muscle cells. The fibroblast PCL model investigates cell-collagen interactions in a 3 dimensional matrix. Fibroblasts maintained in a PCL that remains attached to the underlying tissue culture dish for 4 days transform into myofibroblasts. Cells in an attached rat vessel smooth muscle cell PCL retain their smooth muscle cell phenotype. At 4 days released attached myofibroblast or released attached rat vessel smooth muscle cell PCL are compacted by a mechanism of cell contraction. Lattice contraction by myofibroblast PCL is greater than smooth muscle cell PCL contraction. The actions of vanadate and genistein, which modify protein tyrosine phosphorylation, and ML-7 and Y-27632, which alter actin-myosin filament sliding by the myosin ATPase activity, were studied. Genistein and ML-7 have no affect upon either myofibroblast or smooth muscle cell PCL contraction, indicating protein tyrosine kinase or myosin light chain kinase are not involved in attached delayed released lattice contraction. Vanadate inhibits myofibroblast PCL contraction, indicating myofibroblast lattice contraction is related to protein tyrosine phosphatase activity. Y-27632 inhibits both smooth muscle cell and myofibroblast PCL contraction, suggests both smooth muscle cell and myofibroblast lattice contraction is dependent upon inhibition of myosin light chain phosphatases through Rho associated kinases.

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