Actions of beta-apo-carotenoids in differentiating cells: Differential effects in P19 cells and 3T3-L1 adipocytes

作者：Wang Cynthia X; Jiang Hongfeng; Yuen Jason J; Lee Seung Ah; Narayanasamy Sureshbabu; Curley Robert W Jr; Harrison Earl H; Blaner William S^*

来源：Archives of Biochemistry and Biophysics, 2015, 572: 2-10.

DOI：10.1016/j.abb.2015.01.009

• Retinoid
• All-trans-retinoic acid
• Adipose differentiation
• Obesity
• Transcription
• Gene expression

beta-Apo-carotenoids, including beta-apo-13-carotenone and beta-apo-14'-carotenal, are potent retinoic acid receptor (RAR) antagonists in transactivation assays. We asked how these influence RAR-dependent processes in living cells. Initially, we explored the effects of beta-apo-13-carotenone and beta-apo-14'-carotenal on P19 cells, a mouse embryonal carcinoma cell line that differentiates into neurons when treated with all-trans-retinoic acid. Treatment of P19 cells with either compound failed to block all-trans-retinoic acid induced differentiation. Liquid chromatography tandem mass spectrometry studies, however, established that neither of these beta-apo-carotenoids accumulates in P19 cells. All-trans-retinoic acid accumulated to high levels in P19 cells. This suggests that the uptake and metabolism of beta-apo-carotenoids by some cells does not involve the same processes used for retinoids and that these may be cell type specific. We also investigated the effects of two beta-apo-carotenoids on 3T3-L1 adipocyte marker gene expression during adipocyte differentiation. Treatment of 3T3-L1 adipocytes with either beta-apo-13-carotenone or beta-apo-10'-carotenoic acid, which lacks RAR antagonist activity, stimulated adipocyte marker gene expression. Neither blocked the inhibitory effects of a relatively large dose of exogenous all-trans-retinoic acid on adipocyte differentiation. Our data suggest that in addition to acting as transcriptional antagonists, some beta-apo-carotenoids act through other mechanisms to influence 3T3-L1 adipocyte differentiation. Published by Elsevier Inc.

• 出版日期2015-4-15