Retinoic acid-induced differentiation increases the rate of oxygen consumption and enhances the spare respiratory capacity of mitochondria in SH-SY5Y cells

Xun, Zhiyin; Lee, Do-Yup; Lim, Jormay; Canaria, Christie A.; Barnebey, Adam; Yanonne, Steven M.; McMurray, Cynthia T.

doi:10.1016/j.mad.2012.01.008

Cited by 63 publications

(47 citation statements)

References 50 publications

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“…Importantly, activation of either UCP1 or futile cycles should go hand in hand with the induction of mitochondrial ␤ -oxidation of fatty acids and OXPHOS capacity for a meaningful effect on adipocyte lipid content and whole body energy expenditure to be achieved. It has been previously shown that ATRA enhances OXPHOS and oxygen consumption in SH-SY5Y human neuroblastoma cells, even without any increase in the number of mitochondria or measurable changes in the composition of the electron transport chain ( 42 ). Here, we present evidence of increased OXPHOS capacity and mitochondrial content in 3T3-L1 adipocytes following ATRA exposure, necessary for both UCP1-dependent and UCP1-independent energy dissipation mechanisms.…”

Section: Discussionsupporting

confidence: 56%

All-trans retinoic acid induces oxidative phosphorylation and mitochondria biogenesis in adipocytes

Tourniaire¹,

Mušinović²,

Gouranton³

et al. 2015

Journal of Lipid Research

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Typical white adipocytes are poor in mitochondria and have a low oxidative capacity. Because of this, the contribution of white adipose tissue (WAT) to whole body energy expenditure is considered relatively small. However, there are studies in both humans and rodents documenting a negative association between mitochondrial content in WAT and obesity, as well as examples of nutritional and pharmacological interventions in animals resulting in obesity resistance that associate with increased oxidative capacity in WAT [reviewed in ( 1 )]. Stimulation of mitochondrial biogenesis and oxidative capacity in white adipocytes, when linked to increased energy expenditure in these cells through increased energy uncoupling and/or waste (e.g., futile cycles), emerges therefore as a potential novel target in the control of obesity and its related medical complications ( 1 ).Vitamin A metabolites (i.e., retinoids) modulate the growth and differentiation of a wide range of cells and tissues. Dietary vitamin A and pro-vitamin A are stored as retinyl esters or intracellularly metabolized to retinoic acid (RA), the main active form of vitamin A ( 2 ). There are two isoforms of RA, all-trans -RA (ATRA) and 9-cis -RA, which exert their effects on cell processes through both genomic and nongenomic mechanisms ( 3 ). After the liver, adipose tissue is a major site of vitamin A storage and metabolism, as well as a main target of ATRA action ( 4, 5 ).

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Section: Discussionsupporting

confidence: 56%

All-trans retinoic acid induces oxidative phosphorylation and mitochondria biogenesis in adipocytes

Tourniaire¹,

Mušinović²,

Gouranton³

et al. 2015

Journal of Lipid Research

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“…An increased mitochondrial activity after treatment with retinoids was reported in neuroblastoma cell lines [66], and it was demonstrated that more differentiated neuronal cells exhibit higher oxygen consumption rates as well as metabolic rates [67]. These findings thus support the presumed neuronal differentiation of D283 Med cells treated with ATRA and the capability of CA and CX to enhance this effect.…”

Section: Discussionsupporting

confidence: 61%

The ATRA-induced differentiation of medulloblastoma cells is enhanced with LOX/COX inhibitors: an analysis of gene expression

et al. 2014

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BackgroundA detailed analysis of the expression of 440 cancer-related genes was performed after the combined treatment of medulloblastoma cells with all-trans retinoic acid (ATRA) and inhibitors of lipoxygenases (LOX) and cyclooxygenases (COX). The combinations of retinoids and celecoxib as a COX-2 inhibitor were reported to be effective in some regimens of metronomic therapy of relapsed solid tumors with poor prognosis. Our previous findings on neuroblastoma cells using expression profiling showed that LOX/COX inhibitors have the capability of enhancing the differentiating action of ATRA. Presented study focused on the continuation of our previous work to confirm the possibility of enhancing ATRA-induced cell differentiation in these cell lines via the application of LOX/COX inhibitors. This study provides more detailed information concerning the mechanisms of the enhancement of the ATRA-induced differentiation of medulloblastoma cells.MethodsThe Daoy and D283 Med medulloblastoma cell lines were chosen for this study. Caffeic acid (an inhibitor of 5-LOX) and celecoxib (an inhibitor on COX-2) were used in combined treatment with ATRA. The expression profiling was performed using Human Cancer Oligo GEArray membranes, and the most promising results were verified using RT-PCR.ResultsThe expression profiling of the selected cancer-related genes clearly confirmed that the differentiating effects of ATRA should be enhanced via its combined administration with caffeic acid or celecoxib. This effect was detected in both cell lines. An increased expression of the genes that encoded the proteins participating in induced differentiation and cytoskeleton remodeling was detected in both cell lines in a concentration-dependent manner. This effect was also observed for the CDKN1A gene encoding the p21 protein, which is an important regulator of the cell cycle, and for the genes encoding proteins that are associated with proteasome activity. Furthermore, our results showed that D283 Med cells are significantly more sensitive to treatment with ATRA alone than Daoy cells.ConclusionsThe obtained results on medulloblastoma cell lines are in accordance with our previous findings on neuroblastoma cells and confirm our hypothesis concerning the common mechanism of the enhancement of ATRA-induced cell differentiation in various types of pediatric solid tumors.

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“…Spare reserve capacity reflects the difference between basal and maximal respiratory rate, and this capacity was determined by measuring OCR after treatment with oligomycin to block ATP synthesis and FCCP to uncouple ATP synthesis from the electron transport chain. [15][16][17] The spare reserve capacity in primary AML samples and cell lines was lower than that in normal hematopoietic cells or solid tumor cell lines (Figure 4A-B; summary of results in supplemental Table 3). …”

Section: Aml Cells Have Low Spare Reserve Capacity In Their Respiratomentioning

confidence: 99%

AML cells have low spare reserve capacity in their respiratory chain that renders them susceptible to oxidative metabolic stress

Sriskanthadevan

Jeyaraju

Chung

et al. 2015

Blood

256

228

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Retinoic acid-induced differentiation increases the rate of oxygen consumption and enhances the spare respiratory capacity of mitochondria in SH-SY5Y cells

Cited by 63 publications

References 50 publications

All-trans retinoic acid induces oxidative phosphorylation and mitochondria biogenesis in adipocytes

All-trans retinoic acid induces oxidative phosphorylation and mitochondria biogenesis in adipocytes

The ATRA-induced differentiation of medulloblastoma cells is enhanced with LOX/COX inhibitors: an analysis of gene expression

AML cells have low spare reserve capacity in their respiratory chain that renders them susceptible to oxidative metabolic stress

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