Synergistic induction of acyl-CoA oxidase activity, an indicator of peroxisome proliferation, by arachidonic acid and retinoic acid in Morris hepatoma 7800C1 cells

Sohlenius, Anna‐Karin; Wigren, Jane; Bäckström, Katrin; Andersson, Karin; DePierre, Joseph W.

doi:10.1016/0005-2760(95)00123-t

Cited by 15 publications

(10 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many genes have DR-1 elements that are common targets for transcription factors, HNF4␣, chicken ovalbumin upstream promoter transcription factors (COUP-TF), RXR, or peroxisome proliferator-activated receptor (PPAR). Examples of these genes are apolipoproteins (Apo) AI, AII, B, and CIII (21-23), ornithine transcarbamylase (OTC) (24), medium-chain acyl-CoA dehydrogenase (25), cellular retinal binding protein (CRBPII) (26), acyl Co-oxidase (27), and hepatitis B virus enhancer (28). Thus, potentially the DR-1 site on the HNF1␣ gene can be a target for other nuclear hormone receptors.…”

mentioning

confidence: 99%

Identification of Retinoic Acid-Responsive Elements on the HNF1α and HNF4α Genes

Qian

Cai

Magee

et al. 2000

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

mentioning

confidence: 99%

Identification of Retinoic Acid-Responsive Elements on the HNF1α and HNF4α Genes

Qian

Cai

Magee

et al. 2000

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

“…However, perfluorinated fatty acids (PFFAs), such as perfluorooctanoic and perfluorodecanoic acids (PFOA and PFDA), were shown to be peroxisome proliferators (Sohlenius et al, 1995). PFFAs, like other peroxisome proliferators, can induce hepatomegaly, hepatocyte proliferation, focal hepatocyte necrosis, hypolipidemia and alteration of hepatic lipid metabolism (Vanden-Heuvel et al, 1993).…”

mentioning

confidence: 99%

Inhibition of gap junctional intercellular communication by perfluorinated fatty acids is dependent on the chain length of the fluorinated tail

et al. 1998

View full text Add to dashboard Cite

Perfluorinated fatty acids (PFFAs), such as perfluorooctanoic acid (PFOA) and perfluorodecanoic acid (PFDA), are known peroxisome proliferators and hepatocarcinogens. A causal link between an increase in the oxidative stress by peroxisomes and tumor promotion has been proposed to explain the hepatocarcinogenicity of PFOA and PFDA. However, the down-regulation of gap junctional intercellular communication (GJIC) has also been linked to the tumorpromoting properties of many carcinogens. Therefore, the effect of PFFAs on GJIC in WB-rat liver epithelial cells was determined. The chain length of the PFFAs tested for an effect on GJIC ranged from 2 to 10, 16 and 18 carbons. Carbon lengths of 7 to 10 inhibited GJIC in a dose-response fashion, whereas carbon lengths of 2 to 5, 16 and 18 did not appreciably inhibit GJIC. Inhibition occurred within 15 min and was reversible, with total recovery from inhibition occurring within 30 min after the removal of the compound from the growth medium. This short time of inhibition suggests that GJIC was modified at the post-translational level. Also, this short time period was not long enough for peroxisome proliferation. The post-translational modification of the gap junction proteins was not a consequence of altered phosphorylation as determined by Western blot analysis. Perfluorooctanesulfonic acid also inhibited GJIC in a dose-response fashion similar to PFDA, indicating that the determining factor of inhibition was probably the fluorinated tail, which required 7-10 carbons. Our results suggest that PFFAs could potentially act as hepatocarcinogens at the level of gap junctions in addition to or instead of through peroxisome proliferation.

show abstract

“…Valproate decreased both the DNA binding of the PPARγ and the amount of the receptor within the nuclei of cultured neurons, indicating decreased signaling after valproate treatment. Valproate also elicited the decreased expression of two genes that are known to be regulated by PPAR signaling: ACOX and catalase (Kane et al 2006;Sohlenius et al 1995;Zhao et al 2006a). ACOX and catalase are both located primarily in the matrix of the peroxisome, and they have both been found to contain PPREs in their gene promoters Data are mean ± SE of six independent experiments, expressed as percentage change with respect to the control (nonvalproate-treated cells).…”

Section: Discussionmentioning

confidence: 98%

“…The messenger RNA (mRNA) levels of two genes known to be regulated by the PPAR system-ACOX and catalase (Kane et al 2006;Sohlenius et al 1995;Zhao et al 2006a)-were determined with and without valproate treatment. Both were found to be significantly downregulated in the cells with valproate ( Fig.…”

Section: Gene Expression Datamentioning

confidence: 99%

Neuronal Peroxisome Proliferator-Activated Receptor γ Signaling: Regulation by Mood-Stabilizer Valproate

et al. 2008

View full text Add to dashboard Cite

Valproate (Depakote) remains an effective medication for the prevention and treatment of seizures in epilepsy and of mood symptoms in bipolar disorder. Both of these disorders are severe and debilitating, and both warrant further medication options as well as a better understanding of the side effects associated with their current treatments. Although a number of molecular and cellular processes have been found to be altered by valproate, the medication's therapeutic mechanism has not been fully elucidated. In this paper, peroxisome proliferator-activated receptor (PPAR) signaling was examined to determine valproate's effects on this transcriptional regulatory system in neuronal tissue. PPAR signaling has been found to affect a number of biochemical processes, including lipid metabolism, cellular differentiation, insulin sensitivity, and cell survival. When primary neuronal cultures were treated with valproate, a significant decrease in PPARgamma signaling was observed. This effect was demonstrated through a change in nuclear quantities of PPARgamma receptor and decreased DNA binding of the receptor. Valproate also caused gene expression changes and a change to the peroxisome biochemistry consistent with a decrease of PPARgamma signaling. These biochemical changes may have functional consequences for either valproate's therapeutic mechanism or for its neurological side effects and merit further investigation.

show abstract

Synergistic induction of acyl-CoA oxidase activity, an indicator of peroxisome proliferation, by arachidonic acid and retinoic acid in Morris hepatoma 7800C1 cells

Cited by 15 publications

References 29 publications

Identification of Retinoic Acid-Responsive Elements on the HNF1α and HNF4α Genes

Identification of Retinoic Acid-Responsive Elements on the HNF1α and HNF4α Genes

Inhibition of gap junctional intercellular communication by perfluorinated fatty acids is dependent on the chain length of the fluorinated tail

Neuronal Peroxisome Proliferator-Activated Receptor γ Signaling: Regulation by Mood-Stabilizer Valproate

Contact Info

Product

Resources

About