Human HepG2 and Rat Fao Hepatic-Derived Cell Lines Show Different Responses to Ciprofibrate, a Peroxisome Proliferator: Analysis by Flow Cytometry

HMG-CoA reductase and PPARα are involved in clofibrate-induced apoptosis in human keratinocytes

“…The capability of clofibrate to induce apoptosis has also previously been shown in human and rat hepatoma cells, 8,29,[35][36][37] and in mouse skin cells. 20 Topical treatment with PPARα activators (clofibrate and Wy-14,643), in both subacute and chronic models of hyperproliferation in hairless mice, re- sulted in a substantial decrease in epidermal hyperplasia, also increasing apoptosis.…”

The peroxisome proliferator BR931 kills FaO cells by p53-dependent apoptosis

“…Whereas increased proliferation occurred in the ciprofibrate-treated FaO cells (Passilly et al, 1996), no such effect was observed in rat FaO and mouse MH1C1 hepatoma cells treated with nafenopine (Bayly et al, 1993;Brocard et al, 1993;Passilly et al, 1996); moreover, suppression of cellular growth by nafenopine was observed in rat RH1 and human HTC hepatoma cells (Gill et al, 1995). In addition, although clofibrate induces apoptosis in HepG2 cells (Canuto et al, 1997(Canuto et al, , 1998, the effect of PPs on FaO cell viability remains uncharacterized (Bayly et al, 1993).…”

Maturation of peroxisomes in differentiating human hepatoblastoma cells (HepG2): possible involvement of the peroxisome proliferator-activated receptor α (PPARα)

“…In rat liver treated with hypolipidemic drugs, peroxisome proliferation and the induction of genes encoding peroxisomal β-oxidation enzymes of the inducible pathway are more pronounced in pericentral (zone 3) hepatocytes [46,60], which contain more PPARα protein [31] and are considered to be further differentiated than the cells in the periportal region (zone 1; [57,66]). Hitherto, several studies with hypolipidemic drugs have failed to reveal significant induction of peroxisomes in HepG2 cells [14,54,68]. Interestingly, in ongoing studies we have noted that the response of HepG2 cells to some fibrate drugs is markedly influenced by their state of differentiation (H. Stier, in preparation).…”