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Carcinogenesis Advance Access originally published online on September 26, 2003
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Carcinogenesis, Vol. 25, No. 1, 107-112, January 2004
© Oxford University Press; all rights reserved

CARCINOGENESIS

Cell cross-talk mediates PPAR{alpha} null hepatocyte proliferation after peroxisome proliferator exposure

Teresa C. Weglarz and Eric P. Sandgren1

Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA

Peroxisome proliferator activated receptor{alpha} (PPAR{alpha}) mediates the liver's responses to peroxisome proliferator compounds. These responses include induction of specific hepatic enzymes, peroxisome proliferation and hepatocyte proliferation. PPAR{alpha} null mice, which lack receptor in all cells of the body, do not respond to peroxisome proliferators, indicating that hepatocellular proliferation and other responses require the presence of this receptor in at least some cells. To determine if PPAR{alpha} is required specifically in hepatocytes for each response, we used hepatocyte transplantation to generate chimeric livers composed of PPAR{alpha} null and positive hepatocytes in PPAR{alpha} null or positive hosts. Upon exposure to a peroxisome proliferator, peroxisome proliferation and enzyme induction were restricted to receptor positive hepatocytes, indicating that these responses are cell autonomous with respect to hepatocyte receptor status. However, both PPAR{alpha} null and positive hepatocytes in chimeric livers displayed elevated DNA synthesis regardless of host receptor status, as long as at least some hepatocytes contained receptor. These findings indicate that the mitogenic response to peroxisome proliferators does not require PPAR{alpha} in all hepatocytes.


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