Protein Kinase C Activates Human Lipocalin-type Prostaglandin D Synthase Gene Expression through De-repression of Notch-HES Signaling and Enhancement of AP-2β Function in Brain-derived TE671 Cells

Fujimori, Ko; Kadoyama, Keiichi; Urade, Yoshihiro

doi:10.1074/jbc.m411755200

Cited by 29 publications

(33 citation statements)

References 66 publications

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“…RNA Preparation and Quantification of RNA Level-Total RNA was extracted with Sepasol-RNAI (Nacalai Tesque, Kyoto, Japan), followed by further purification with an RNeasy Purification System (Qiagen, Hilden, Germany) (26). The firststrand cDNAs were synthesized from 1 g of total RNA with random hexamer and ReverTra Ace Reverse Transcriptase (Toyobo, Osaka, Japan) at 42°C for 60 min after the initial denaturation at 72°C for 3 min, followed by heat denaturation of enzyme at 99°C for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Suppression of Adipocyte Differentiation by Aldo-keto Reductase 1B3 Acting as Prostaglandin F2α Synthase

Fujimori

Ueno

Nagata

et al. 2010

Journal of Biological Chemistry

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Prostaglandin (PG) F 2␣ suppresses adipocyte differentiation by inhibiting the function of peroxisome proliferatoractivated receptor ␥. However, PGF 2␣ synthase (PGFS) in adipocytes remains to be identified. Here, we studied the expression of members of the aldo-keto reductase (AKR) 1B family acting as PGFS during adipogenesis of mouse 3T3-L1 cells. AKR1B3 mRNA was expressed in preadipocytes, and its level increased about 4-fold at day 1 after initiation of adipocyte differentiation, and then quickly decreased the following day to a level lower than that in the preadipocytes. In contrast, the mRNA levels of Akr1b8 and 1b10 were clearly lower than that level of Akr1b3 in preadipocytes and remained unchanged during adipogenesis. The transient increase in Akr1b3 during adipogenesis was also observed by Western blot analysis. The mRNA for the FP receptor, which is selective for PGF 2␣ , was also expressed in preadipocytes. Its level increased about 2-fold within 1 h after the initiation of adipocyte differentiation and was maintained at almost the same level throughout adipocyte differentiation. The small interfering RNA for Akr1b3, but not for Akr1b8 or 1b10, suppressed PGF 2␣ production and enhanced the expression of adipogenic genes such as peroxisome proliferator-activated receptor ␥, fatty acid-binding protein 4 (aP2), and stearoylCoA desaturase. Moreover, an FP receptor agonist, Fluprostenol, suppressed the expression of those adipogenic genes in 3T3-L1 cells; whereas an FP receptor antagonist, AL-8810, efficiently inhibited the suppression of adipogenesis caused by the endogenous PGF 2␣ . These results indicate that AKR1B3 acts as the PGFS in adipocytes and that AKR1B3-produced PGF 2␣ suppressed adipocyte differentiation by acting through FP receptors.

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Section: Methodsmentioning

confidence: 99%

Suppression of Adipocyte Differentiation by Aldo-keto Reductase 1B3 Acting as Prostaglandin F2α Synthase

Fujimori

Ueno

Nagata

et al. 2010

Journal of Biological Chemistry

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“…However, the transcriptional regulation of AP-2β is still unknown. It was recently reported that the transcriptional activity of AP-2α (another member of the AP2 family) is regulated by PKcµ, and that PKcα enhances the activation of AP-2β (30,31). These data led to us to hypothesize that PKcµ may regulate the activity of AP-2β in adipocytes.…”

Section: Introductionmentioning

confidence: 99%

Postprandial activation of protein kinase Cï¿½ regulates the expression of adipocytokines via the transcription factor AP-2β

Kondo

Ugi²,

Morino³

et al. 2011

Int J Mol Med

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Abstract. Abnormal secretion of adipocytokines promotes atherosclerosis, diabetes and insulin resistance, and is mainly induced by adipocyte hypertrophy. Recently, the circulating adipocytokine concentrations were reported to change in the postprandial period, as the levels of TNFα, IL-6 IL-8 and McP-1 increased after a meal, whereas that of adiponectin decreased. These data suggest that prandial modulation of cytokines may be involved in the pathogenesis of atherosclerosis in type 2 diabetes. However, the regulatory mechanism of such change is still unclear. In the present study, we identified this mechanism with a special focus on the functions of protein kinase c (PKc) and of the transcription factor AP-2β, both of which are associated with the pathophysiology of adipocytokine regulation. PKcµ was highly phosphorylated in the re-feeding condition compared to the fasting condition in mouse adipose tissue, while other PKc isoforms remained unchanged. Furthermore, overexpression of PKcµ in 3T3-L1 adipocytes, but not other PKc isoforms, positively regulated the mRNA expression and promoter activity of McP-1 and IL-6, and negatively regulated those of adiponectin. AP-2β had similar effects on the expression and promoter activity of these adipocytokines. Interestingly, overexpression of PKcµ enhanced the stimulatory and inhibitory effects of AP-2β on the expression of these adipocytokines. Finally, PKcµ could not activate a mutant McP-1 promoter lacking the AP-2β binding domain. Our results suggest that postprandial activation of PKcµ plays a role in disordered postprandial adipocytokine expression through AP-2β.

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“…Chromatin immunoprecipitation (ChIP) assays were performed as described previously (7). Briefly, 3T3-L1 cells were caused to differentiate into adipocytes in the presence of the potent PPAR␥ agonist troglitazone (10 M) as the positive control for 6 days.…”

Section: Cell Culture Mouse Adipocytic 3t3-l1 Cells and Human Hela Cmentioning

confidence: 99%

Very long-chain-fatty acids enhance adipogenesis through coregulation of Elovl3 and PPARγ in 3T3-L1 cells

Kobayashi

Fujimori

2012

American Journal of Physiology-Endocrinology and Metabolism

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Protein Kinase C Activates Human Lipocalin-type Prostaglandin D Synthase Gene Expression through De-repression of Notch-HES Signaling and Enhancement of AP-2β Function in Brain-derived TE671 Cells

Cited by 29 publications

References 66 publications

Suppression of Adipocyte Differentiation by Aldo-keto Reductase 1B3 Acting as Prostaglandin F2α Synthase

Suppression of Adipocyte Differentiation by Aldo-keto Reductase 1B3 Acting as Prostaglandin F2α Synthase

Postprandial activation of protein kinase Cï¿½ regulates the expression of adipocytokines via the transcription factor AP-2β

Very long-chain-fatty acids enhance adipogenesis through coregulation of Elovl3 and PPARγ in 3T3-L1 cells

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