Arachidonic Acid Reverses Xanthohumol-Induced Insufficiency in a Human First-Trimester Extravillous Trophoblast Cell Line (HTR-8/SVneo Cells)

• Type: Article in International Scientific Journal
• Date: 2018

Authors

Correia Branco, A (Author) Other; Elisa Keating (Author) FMUP; Martel, F (Author) FMUP

Journal

Title: Reproductive Sciences

Vol. 25

Pages: 1394-1405

ISSN: 1933-7191

Publisher: SAGE

Indexing

ISI Web of Knowledge - 2 Citations

Scopus - 3 Citations

Other information

Authenticus ID: P-00P-HDT

DOI: 10.1177/1933719117746762

Abstract (EN): We previously described a negative effect of xanthohumol (XN) upon placentation-related processes. We aimed to better characterize this effect by investigating the effect of XN upon the uptake of arachidonic acid (ARA), a crucial nutrient during pregnancy, by the HTR-8/SVneo human first-trimester extravillous trophoblast cell line and its relationship with the negative effect of XN upon placentation-related processes. Uptake of C-14-ARA (100 nM) was time dependent and inhibited by short-term (26 minutes) or long-term (24 hours) exposure to XN. Xanthohumol (24 hours; 5 mu M) behaved as an uncompetitive inhibitor of C-14-ARA uptake; the mammalian target of rapamycin, tyrosine kinases, and c-Jun N-terminal kinases intracellular pathways were involved in this effect; and it markedly reduced long-chain acyl-CoA synthetase 1 messenger RNA levels. Moreover, the effects of XN (24 hours; 5 mu M) upon cell proliferation, culture growth, migration, viability, and apoptosis index were prevented by high extracellular ARA but not by the peroxisome proliferator-activated receptor- (PPAR-) agonist rosiglitazone. We thus conclude that ARA is an essential nutrient regulating cell viability, proliferation, culture growth, migration, and apoptosis of HTR-8/SVneo cells and that the deleterious effects of XN involve inhibition of ARA cellular uptake but appears to be independent of PPAR- activation.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 12