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Toxicological Sciences 68, 270-274 (2002)
Copyright © 2002 by the Society of Toxicology

FORUM

Evidence for Cross Talk between PPAR{alpha} and p38 MAP Kinase

Ruth A. Roberts,1

Syngenta CTL, Alderley Park, Macclesfield, SK10 4TJ, United Kingdom

Received February 4, 2002; accepted March 27, 2002

The first 150 words of the full text of this article appear below.


   INTRODUCTION
 
The evidence implicating the peroxisome proliferator activated receptor (PPAR{alpha}) in peroxisome proliferator (PP)-induced rodent hepatocarcinogenesis is compelling. However, the question that remains is "Which genes are regulated by PPAR{alpha} to perturb hepatocyte proliferation and apoptosis leading to PP-induced rodent hepatocarcinogenesis?" Despite extensive research, there are no convincing gene targets that display the required link with causality and sufficient specificity. However, some laboratories suggest a role for p38 mitogen-activated protein (MAP) kinase in mediating PP-induced hepatocyte survival and proliferation but not peroxisome proliferation. Thus, cross talk between the p38 and PPAR{alpha} signaling pathways may facilitate the growth but not the biochemical changes seen in response to this important class of xenobiotics.

The discovery of the PPAR{alpha} in 1990 (Issemann and Green, 1990Go) stimulated much research worldwide aimed at elucidating its role in mediating the response to the PP class of nongenotoxic hepatocarcinogens (reviewed in Auwerx, 1992Go; Kliewer et . . . [Full Text of this Article]


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