Up‐regulation of cyclooxygenase‐1 in neuroblastoma cell lines by retinoic acid and corticosteroids

Schneider, Norbert; Lanz, Stefan; Ramer, Robert; Schaefer, Dirk J.; Goppelt‐Struebe, Margarete

doi:10.1046/j.1471-4159.2001.00264.x

Cited by 35 publications

(23 citation statements)

References 48 publications

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“…Dexamethasone causes a dose-and time-dependent increase in expression and activity of prostaglandin D2 synthase in neuronal cultures (Garcia-Fernandez et al 2000) and dexamethasone or corticosterone treatment increases the pro-inflammatory leukotriene synthesis enzyme 5-lipoxygenase in both the hippocampus (Uz et al 1999) and macrophages (Riddick et al 1997). Finally, dexamethasone alone or more robustly in conjunction with retinoic acid, causes increased COX-1 expression in neuroblastoma cell lines (Schneider et al 2001).…”

Section: 3mentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

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In recent years the classic view that glucocorticoids, the adrenal steroids secreted during stress, are universally anti-inflammatory has been challenged at a variety of levels. It was first observed that under some circumstances, acute GC exposure could have pro-inflammatory effects on the peripheral immune response. More recently, chronic exposure to GCs has been found to have pro-inflammatory effects on the specialized immune response to injury in the central nervous system. Here we review the evidence that in some cases, glucocorticoids can increase pro-inflammatory cell migration, cytokine production, and even transcription factor activity in the brain. We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings.

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Section: 3mentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

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“…Design and statistical analyses Studies were designed as reported by others using cell line models (Chiaramonte et al, 1998;Schneider et al, 2001). Thus, each experiment was replicated using triplicate (or a greater number of replicate) assays from duplicate cultures for each test condition.…”

Section: Secondary Antibody Was Alexa Fluor 680 Goat Anti-rabbit Igg mentioning

confidence: 99%

“…Total protein was determined using the BCA assay (Pierce Chemical Co., Rockford, IL, USA) and 20 mg protein was loaded per lane on SDS PAGE. Resolved proteins were transferred to nitrocellulose and detected in Western blot using (1/1000) polyclonal rabbit anti-PPAR-g antibody or rabbit anti-GLUT-4 antibody, and secondary antibody (1/5000) Alexa Fluor 680 goat anti-rabbit IgG and scanned on an infra-red fluorescence imager (Odyssey; LI-COR, Inc., Lincoln, NE, USA).Design and statistical analyses Studies were designed as reported by others using cell line models (Chiaramonte et al, 1998;Schneider et al, 2001). Thus, each experiment was replicated using triplicate (or a greater number of replicate) assays from duplicate cultures for each test condition.…”

mentioning

confidence: 99%

Regulation of lipid accumulation in 3T3-L1 cells: insulin-independent and combined effects of fatty acids and insulin

Kokta

Strat

Papasani

et al. 2008

Animal

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The insulin-independent and combined effects of fatty acids (FA; linoleic and oleic acids) and insulin in modulating lipid accumulation and adipogenesis in 3T3-L1 cells was investigated using a novel protocol avoiding the effects of a complex hormone 'induction' mixture. 3T3-L1 cells were cultured in Dulbecco's modified Eagle's medium (DMEM) plus serum (control) or in DMEM plus either 0.3 mmol/l linoleic or oleic acids with 0.3 mmol/l FA-free bovine serum albumin in the presence or absence of insulin. Cells were cultured for 4 to 8 days and cell number, lipid accumulation, peroxisome proliferator-activated receptor-gamma (PPAR-g) and glucose transporter 4 (GLUT-4) protein expression were determined. Cell number appeared to be decreased in comparison with control cultures. In both oleic acid and linoleic acid-treated cells, notably in the absence (and presence) of insulin, oil-red O stain-positive cells showed abundant lipid. The percentage of cells showing lipid accumulation was greater in FA-treated cultures compared with control cells grown in DMEM plus serum (P , 0.001). Treatment with both linoleic and oleic acid-containing media evoked higher levels of PPAR-g than observed in control cultures (P , 0.05). GLUT-4 protein also increased in response to treatment with both linoleic and oleic acid-containing media (P , 0.001). Lipid accumulation in 3T3-L1 cells occurs in response to either oleic or linoleic acids independently of the presence of insulin. Both PPAR-g and GLUT-4 protein expression were stimulated. Both proteins are considered markers of adipogenesis, and these observations suggest that these cells had entered the physiological state broadly accepted as differentiated. Furthermore, 3T3-L1 cells can be induced to accumulate lipid in a serum-free medium supplemented with FA, without the use of induction protocols using complex hormone mixtures. We have demonstrated a novel model for the study of lipid accumulation that will improve the understanding of adipogenesis in adipocyte lineage cells.Keywords: adipogenesis, fatty acids, GLUT-4, insulin, PPAR-g IntroductionProgression to lipid storage in adipocytes is characterised by two distinct phases. In the first step of hyperplastic expansion, progenitor cells are thought to become committed to the adipocyte lineage, after which they cannot revert back to a less differentiated 'stem-like' cell (Thompson et al., 1998;Boone et al., 2000). Once committed, adipoblasts undergo an exponential replication phase that terminates and the cell cycle arrests at gap 1 (G1). Early markers of differentiation, such as lipoprotein lipase (LPL) are then expressed, and these cells, known as preadipocytes, may then undergo proliferation (Boone et al., 2000). After preadipocytes stop proliferating, late markers of differentiation, such as glycerol-3-phosphate dehydrogenase (GPDH) and fatty acid synthetase (FAS) are detected. Cells then begin lipid accumulation in the cytosol at which time cells are termed adipocytes (Boone et al., 2000).Much of our understanding of these proc...

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“…However, retinoid isomers including ATRA and 9-cis-RA were described to induce COX-1 in human premonocytic U937 cells 20 and human Arsenic inhibits ATRA-induced COX-1 in NB4 cells A Habib et al neuroblastoma cell lines. 21 ATRA-induced COX-1 upregulation may be mediated by the Sp1 transcription factor, which is significantly upregulated during myeloid differentiation, and has been reported to mediate ATRA responsiveness of several genes devoid of RAR-responsive element (RARE) motifs. [27][28][29] In that sense, the COX-1 promoter contains two Sp1-binding sequences but no canonical RARE.…”

Section: Discussionmentioning

confidence: 99%

“…[17][18][19] Retinoid isomers including ATRA and 9-cis-RA were described to induce COX-1 in human premonocytic U937 cells. 20 Retinoic acid was also described to induce COX-1 in human neuroblastoma cell lines 21 and COX-2 in synergy with platelet activating factor. 22 We have recently demonstrated that ATRA induces COX-1 but not COX-2 in NB4 cells and in blasts from patients with APL.…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide inhibits ATRA-induced prostaglandin E2 and cyclooxygenase-1 in NB4 cells, a model of acute promyelocytic leukemia

et al. 2008

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In acute promyelocytic leukemia (APL), all-trans retinoic acid (ATRA) triggers cell differentiation, while arsenic trioxide (As 2 O 3 ) generates partial differentiation and apoptosis. Animal and human studies suggest that newly diagnosed APL patients can be cured using As 2 O 3 combined with ATRA. Cyclooxygenases are involved in prostaglandins and thromboxane synthesis. We have recently demonstrated that ATRA induces cyclooxygenase-1 (COX-1) expression and prostaglandin synthesis in NB4 cells and in blasts from patients with APL. In the present study we investigated the effect of ATRA and As 2 O 3 co-treatment on COX-1 expression and prostaglandin formation and tested the effect of the COX-1/COX-2 nonselective inhibitor indomethacin on cell differentiation. Arsenic treatment of NB4 cells resulted in a partial but significant reduction of ATRA-dependent induction of COX-1 expression and activity. Pretreatment of NB4 cells with indomethacin significantly impaired ATRA/As 2 O 3 -induced differentiation, as assessed by cell morphology, nitroblue tetrazolium test or CD11c expression. PGE 2 reversed the negative effect of indomethacin on differentiation of ATRA/As 2 O 3 -treated NB4 cells. In conclusion, COX-1 contributes to ATRA-dependent maturation of NB4 cells and is affected by As 2 O 3 . These results also suggest that nonsteroidal antiinflammatory drugs should be avoided in APL patients treated with the combination of ATRA and As 2 O 3 .

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Up‐regulation of cyclooxygenase‐1 in neuroblastoma cell lines by retinoic acid and corticosteroids

Cited by 35 publications

References 48 publications

An inflammatory review of glucocorticoid actions in the CNS

An inflammatory review of glucocorticoid actions in the CNS

Regulation of lipid accumulation in 3T3-L1 cells: insulin-independent and combined effects of fatty acids and insulin

Arsenic trioxide inhibits ATRA-induced prostaglandin E2 and cyclooxygenase-1 in NB4 cells, a model of acute promyelocytic leukemia

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