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© The Rockefeller University Press, 0021-9525/1997//1477 $5.00
The Journal of Cell Biology, Volume 139, Number 6, , 1997 1477-1484

Article

Sarcomeric Gene Expression and Contractility in Myofibroblasts



D.C. Ghislaine Mayer and Leslie A. Leinwand

Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Colorado 80309

Myofibroblasts are unusual cells that share morphological and functional features of muscle and nonmuscle cells. Such cells are thought to control liver blood flow and kidney glomerular filtration rate by having unique contractile properties. To determine how these cells achieve their contractile properties and their resemblance to muscle cells, we have characterized two myofibroblast cell lines. Here, we demonstrate that myofibroblast cell lines from kidney mesangial cells (BHK) and liver stellate cells activate extensive programs of muscle gene expression including a wide variety of muscle structural proteins. In BHK cells, six different striated myosin heavy chain isoforms and many thin filament proteins, including troponin T and tropomyosin are expressed. Liver stellate cells express a limited subset of the muscle thick filament proteins expressed in BHK cells. Although these cells are mitotically active and do not morphologically differentiate into myotubes, we show that MyoD and myogenin are expressed and functional in both cell types. Finally, these cells contract in response to endothelin-1 (ET-1); and we show that ET-1 treatment increases the expression of sarcomeric myosin.

Abbreviations used in this paper: ET-1, endothelin 1; MLC, myosin light chain; MRF, myogenic regulatory factors; MyHC, myosin heavy chain isoforms; NGS, normal goat serum; TnT, troponin T.

Address all correspondence to Leslie A. Leinwand, Department of Molecular, Cellular and Developmental Biology, University of Colorado, Campus Box 347, Boulder, CO 80309-0347. Tel.: (303) 492-7606. Fax: (303) 492-8907. E-mail: leinwand{at}stripe.colorado.edu

The authors acknowledge C. Saez for initiating this project. We thank M. Buvoli, B. Tompkins, B. Lu, and K. Haubold for assistance with figures. We thank K.L. Vikstrom and O. Roopnarine for critical reading of the manuscript. The authors would like to thank T. Giddings for assistance with electron microscopy.

D.C.G. Mayer was supported by National Institutes of Health grant No. GM29090. The research was supported by NIH grant No. GM29090 to L.A. Leinwand. This work is submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Sue Golding Graduate Division of Medical Sciences, Albert Einstein College of Medicine, Yeshiva University (New York).


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