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Propyl gallate inhibits adipogenesis by stimulating extracellular signal-related kinases in human adipose tissue-derived mesenchymal stem cells.

Lee JE, Kim JM, Jang HJ, Lim SY, Choi SJ, Lee NH, Suh PG, Choi UK - Mol. Cells (2015)

Bottom Line: Propyl gallate (PG) used as an additive in various foods has antioxidant and anti-inflammatory effects.In addition, PG significantly reduced the expression of adipocyte-specific markers including peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT enhancer binding protein-α (C/EBP-α), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein 2 (aP2).Taken together, these results suggest a novel effect of PG on adipocyte differentiation in hAMSCs, supporting a negative role of ERK1/2 pathway in adipogenic differentiation.

View Article: PubMed Central - PubMed

Affiliation: School of Nano-Bioscience and Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan 689-798, Korea.

ABSTRACT
Propyl gallate (PG) used as an additive in various foods has antioxidant and anti-inflammatory effects. Although the functional roles of PG in various cell types are well characterized, it is unknown whether PG has effect on stem cell differentiation. In this study, we demonstrated that PG could inhibit adipogenic differentiation in human adipose tissue-derived mesenchymal stem cells (hAMSCs) by decreasing the accumulation of intracellular lipid droplets. In addition, PG significantly reduced the expression of adipocyte-specific markers including peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT enhancer binding protein-α (C/EBP-α), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein 2 (aP2). PG inhibited adipogenesis in hAMSCs through extracellular regulated kinase (ERK) pathway. Decreased adipogenesis following PG treatment was recovered in response to ERK blocking. Taken together, these results suggest a novel effect of PG on adipocyte differentiation in hAMSCs, supporting a negative role of ERK1/2 pathway in adipogenic differentiation.

No MeSH data available.


Related in: MedlinePlus

Propyl gallate (PG) inhibits PPAR-γ activity. HEK293 cells were co-transfected with PPREx3-tk-luciferase reporter plasmid, the Renilla luciferase plasmid, and the PPAR-γ2 expression vector. At 12 h post transfection, cells were treated with 100 nM rosiglitazone and PG for 36 h. Ligand-dependent transcriptional activity was measured by dual-luciferase assay. Data are presented as the ratio of firefly luciferase activity to Renilla luciferase activity. Values are presented as mean ± SD. *p < 0.05 compared to control; PPAR-γ peroxisome proliferator-activated receptor-γ.
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f3-molce-38-4-336: Propyl gallate (PG) inhibits PPAR-γ activity. HEK293 cells were co-transfected with PPREx3-tk-luciferase reporter plasmid, the Renilla luciferase plasmid, and the PPAR-γ2 expression vector. At 12 h post transfection, cells were treated with 100 nM rosiglitazone and PG for 36 h. Ligand-dependent transcriptional activity was measured by dual-luciferase assay. Data are presented as the ratio of firefly luciferase activity to Renilla luciferase activity. Values are presented as mean ± SD. *p < 0.05 compared to control; PPAR-γ peroxisome proliferator-activated receptor-γ.

Mentions: PPAR-γ is a critical adipogenes is transcription factor (Rosen et al., 2000; Spiegelman, 1998). Some natural products can regulate adipogenesis by modulating PPAR-γ activity (Gong et al., 2009; Saito et al., 2009; Shang et al., 2007). Based on these reports, we tested whether PG could inhibit adipocyte differentiation by regulating PPAR-γ activity. Because the transfection efficiency of hAMSCs was very low, we used HEK293 cells to examine the effect of PG on PPAR-γ activity. HEK293 cells were co-transfected with a PPREx3-tk-luciferase reporter plasmid and PPAR-γ2 expression vector. We used rosiglitazone, a synthetic PPAR-γ ligand, as a positive control. At 36 h post treatment, rosiglitazone (100 nM) significantly (p < 0.05) increased the activity of PPAR-γ (Fig. 3). Co-treatment with PG reduced the transcriptional activity of PPAR-γ in a dose-dependent manner (Fig. 3). These results suggest that PG can suppress adipogenesis of hAMSCs by inhibiting PPAR-γ activity.


Propyl gallate inhibits adipogenesis by stimulating extracellular signal-related kinases in human adipose tissue-derived mesenchymal stem cells.

Lee JE, Kim JM, Jang HJ, Lim SY, Choi SJ, Lee NH, Suh PG, Choi UK - Mol. Cells (2015)

Propyl gallate (PG) inhibits PPAR-γ activity. HEK293 cells were co-transfected with PPREx3-tk-luciferase reporter plasmid, the Renilla luciferase plasmid, and the PPAR-γ2 expression vector. At 12 h post transfection, cells were treated with 100 nM rosiglitazone and PG for 36 h. Ligand-dependent transcriptional activity was measured by dual-luciferase assay. Data are presented as the ratio of firefly luciferase activity to Renilla luciferase activity. Values are presented as mean ± SD. *p < 0.05 compared to control; PPAR-γ peroxisome proliferator-activated receptor-γ.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4400308&req=5

f3-molce-38-4-336: Propyl gallate (PG) inhibits PPAR-γ activity. HEK293 cells were co-transfected with PPREx3-tk-luciferase reporter plasmid, the Renilla luciferase plasmid, and the PPAR-γ2 expression vector. At 12 h post transfection, cells were treated with 100 nM rosiglitazone and PG for 36 h. Ligand-dependent transcriptional activity was measured by dual-luciferase assay. Data are presented as the ratio of firefly luciferase activity to Renilla luciferase activity. Values are presented as mean ± SD. *p < 0.05 compared to control; PPAR-γ peroxisome proliferator-activated receptor-γ.
Mentions: PPAR-γ is a critical adipogenes is transcription factor (Rosen et al., 2000; Spiegelman, 1998). Some natural products can regulate adipogenesis by modulating PPAR-γ activity (Gong et al., 2009; Saito et al., 2009; Shang et al., 2007). Based on these reports, we tested whether PG could inhibit adipocyte differentiation by regulating PPAR-γ activity. Because the transfection efficiency of hAMSCs was very low, we used HEK293 cells to examine the effect of PG on PPAR-γ activity. HEK293 cells were co-transfected with a PPREx3-tk-luciferase reporter plasmid and PPAR-γ2 expression vector. We used rosiglitazone, a synthetic PPAR-γ ligand, as a positive control. At 36 h post treatment, rosiglitazone (100 nM) significantly (p < 0.05) increased the activity of PPAR-γ (Fig. 3). Co-treatment with PG reduced the transcriptional activity of PPAR-γ in a dose-dependent manner (Fig. 3). These results suggest that PG can suppress adipogenesis of hAMSCs by inhibiting PPAR-γ activity.

Bottom Line: Propyl gallate (PG) used as an additive in various foods has antioxidant and anti-inflammatory effects.In addition, PG significantly reduced the expression of adipocyte-specific markers including peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT enhancer binding protein-α (C/EBP-α), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein 2 (aP2).Taken together, these results suggest a novel effect of PG on adipocyte differentiation in hAMSCs, supporting a negative role of ERK1/2 pathway in adipogenic differentiation.

View Article: PubMed Central - PubMed

Affiliation: School of Nano-Bioscience and Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan 689-798, Korea.

ABSTRACT
Propyl gallate (PG) used as an additive in various foods has antioxidant and anti-inflammatory effects. Although the functional roles of PG in various cell types are well characterized, it is unknown whether PG has effect on stem cell differentiation. In this study, we demonstrated that PG could inhibit adipogenic differentiation in human adipose tissue-derived mesenchymal stem cells (hAMSCs) by decreasing the accumulation of intracellular lipid droplets. In addition, PG significantly reduced the expression of adipocyte-specific markers including peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT enhancer binding protein-α (C/EBP-α), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein 2 (aP2). PG inhibited adipogenesis in hAMSCs through extracellular regulated kinase (ERK) pathway. Decreased adipogenesis following PG treatment was recovered in response to ERK blocking. Taken together, these results suggest a novel effect of PG on adipocyte differentiation in hAMSCs, supporting a negative role of ERK1/2 pathway in adipogenic differentiation.

No MeSH data available.


Related in: MedlinePlus