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. 2003 May;23(9):3052–3066. doi: 10.1128/MCB.23.9.3052-3066.2003

FIG. 1.

FIG. 1.

FIG. 1.

DCA activates ERK1/2 and JNK1/2 in primary hepatocytes. Hepatocytes were isolated and cultured as described in “Methods.” Twenty-four hours after plating, cells were treated with either vehicle or vehicle containing the MEK1/2 inhibitor PD98059 (final concentration, 50 μM). Thirty minutes after PD98059 treatment, cells were exposed to bile acid (final concentrations: rat, 50 μM; mouse, 150 μM). At the indicated times after bile acid exposure, cells were lysed in SDS-PAGE sample buffer containing bromophenol blue, boiled, and subjected to SDS-PAGE followed by transfer to nitrocellulose. Immunoblotting was performed as described in “Methods” (39, 40, 41). (A) DCA increases ERK1/2 phosphorylation in rat hepatocytes that is blocked by PD98059. (B) DCA increases JNK1/2 phosphorylation in rat hepatocytes. (C) DCA weakly increases p38 activity in rat hepatocytes that is not altered by PD98059. The JNK1/2/3 inhibitor SP600125 did not alter the activation of either ERK1/2 or p38α (data not shown). Data in all panels are from a representative study (n = 3).