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Research Article Free access | 10.1172/JCI117497

Induction of beta-platelet-derived growth factor receptor in rat hepatic lipocytes during cellular activation in vivo and in culture.

L Wong, G Yamasaki, R J Johnson, and S L Friedman

University of California, San Francisco Liver Center Laboratory 94110.

Find articles by Wong, L. in: PubMed | Google Scholar

University of California, San Francisco Liver Center Laboratory 94110.

Find articles by Yamasaki, G. in: PubMed | Google Scholar

University of California, San Francisco Liver Center Laboratory 94110.

Find articles by Johnson, R. in: PubMed | Google Scholar

University of California, San Francisco Liver Center Laboratory 94110.

Find articles by Friedman, S. in: PubMed | Google Scholar

Published October 1, 1994 - More info

Published in Volume 94, Issue 4 on October 1, 1994
J Clin Invest. 1994;94(4):1563–1569. https://doi.org/10.1172/JCI117497.
© 1994 The American Society for Clinical Investigation
Published October 1, 1994 - Version history
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Abstract

A consistent response to liver injury is the activation of resident mesenchymal cells known as lipocytes (Ito, fat-storing cells) into a proliferating cell type. In cultured lipocytes, platelet-derived growth factor (PDGF) is the most potent proliferative cytokine, but requires the activation-dependent expression of its receptor protein (Friedman, S. L., and M. J. P. Arthur. 1989. J. Clin. Invest. 84:1780-1785); the role of PDGF receptor (PDGFR) in liver injury is unknown. We have examined PDGFR gene expression in freshly isolated lipocytes during liver injury and correlated these findings with a culture model of cellular activation. Whereas lipocytes from normal rats had no detectable transcript for the beta-PDGFR subunit, this mRNA was induced within 1 h after a dose of carbon tetrachloride (CCl4). In contrast, alpha subunit mRNA was detected in normal cells, but was unchanged after liver injury. Similar results were observed in lipocytes from bile duct-obstructed rats, although beta-PDGFR induction was less marked. By immunoblot, induction of beta-PDGFR protein in lipocytes isolated from CCl4-treated animals correlated with mRNA increases. In contrast to lipocytes, endothelial cells from normal liver expressed low levels of alpha- and beta-receptor subunit mRNA, which did not increase with injury. Using a beta-PDGFR antibody, receptor protein could be identified within fibrotic septa in CCl4-treated animals in regions where cells expressed proliferating cell nuclear antigen (PCNA). In cultured lipocytes activated by growth on uncoated plastic, beta-PDGFR transcripts appeared within 3 d after plating, which coincided with the onset of cellular proliferation. In contrast, quiescent cells in suspension culture had no detectable beta-PDGFR mRNA. These results indicate that beta-PDGF receptor induction by lipocytes is an early event during hepatic injury in vivo and in primary culture.

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