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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) activates phosphorylation of ERK1/2 and p38 in hAMSCs. (A) hAMSCs were treated with 10 μM PG under serum-free conditions. Cell lysates were prepared at different time points as indicated. ERK1/2, p38, and JNK1 phosphorylation was examined by immunoblotting; (B) hAMSCs were incubated with or without PG (10 μM) in AIM. Cell lysates were subjected to immunoblot analysis. ERK1/2 and p38 phosphorylation was stimulated by PG treatment; (C) hAMSCs were treated with or without PG (10 μM) under adipogenic differentiation condition. ERK1/2 and p38 phosphorylations as well as ERK2 and β-actin expression were examined. β-actin was used as loading control. ERK: extracellular regulated kinase; JNK: Jun-kinase; hAMSCs: human adipose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium.
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f4-molce-38-4-336: Propyl gallate (PG) activates phosphorylation of ERK1/2 and p38 in hAMSCs. (A) hAMSCs were treated with 10 μM PG under serum-free conditions. Cell lysates were prepared at different time points as indicated. ERK1/2, p38, and JNK1 phosphorylation was examined by immunoblotting; (B) hAMSCs were incubated with or without PG (10 μM) in AIM. Cell lysates were subjected to immunoblot analysis. ERK1/2 and p38 phosphorylation was stimulated by PG treatment; (C) hAMSCs were treated with or without PG (10 μM) under adipogenic differentiation condition. ERK1/2 and p38 phosphorylations as well as ERK2 and β-actin expression were examined. β-actin was used as loading control. ERK: extracellular regulated kinase; JNK: Jun-kinase; hAMSCs: human adipose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium.

Mentions: Recent studies have shown that several compounds can modulate adipogenic differentiation by regulating MAPK activity, highlighting the central roles of MAPKs in adipocyte differentiation. Based on these reports, we determined whether PG could activate MAPKs in hAMSCs. In serum starvation condition, PG (10 M) induced ERK1/2 and p38 phosphorylation, but not JNK phosphorylation (Fig. 4A). In addition, treatment with PG (10 M) potentiated ERK1/2 and p38 phosphorylation under AIM conditions compared to treatment with vehicle control (Figs. 4B and 4C).


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) activates phosphorylation of ERK1/2 and p38 in hAMSCs. (A) hAMSCs were treated with 10 μM PG under serum-free conditions. Cell lysates were prepared at different time points as indicated. ERK1/2, p38, and JNK1 phosphorylation was examined by immunoblotting; (B) hAMSCs were incubated with or without PG (10 μM) in AIM. Cell lysates were subjected to immunoblot analysis. ERK1/2 and p38 phosphorylation was stimulated by PG treatment; (C) hAMSCs were treated with or without PG (10 μM) under adipogenic differentiation condition. ERK1/2 and p38 phosphorylations as well as ERK2 and β-actin expression were examined. β-actin was used as loading control. ERK: extracellular regulated kinase; JNK: Jun-kinase; hAMSCs: human adipose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium.
© Copyright Policy
Related In: Results  -  Collection

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

f4-molce-38-4-336: Propyl gallate (PG) activates phosphorylation of ERK1/2 and p38 in hAMSCs. (A) hAMSCs were treated with 10 μM PG under serum-free conditions. Cell lysates were prepared at different time points as indicated. ERK1/2, p38, and JNK1 phosphorylation was examined by immunoblotting; (B) hAMSCs were incubated with or without PG (10 μM) in AIM. Cell lysates were subjected to immunoblot analysis. ERK1/2 and p38 phosphorylation was stimulated by PG treatment; (C) hAMSCs were treated with or without PG (10 μM) under adipogenic differentiation condition. ERK1/2 and p38 phosphorylations as well as ERK2 and β-actin expression were examined. β-actin was used as loading control. ERK: extracellular regulated kinase; JNK: Jun-kinase; hAMSCs: human adipose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium.
Mentions: Recent studies have shown that several compounds can modulate adipogenic differentiation by regulating MAPK activity, highlighting the central roles of MAPKs in adipocyte differentiation. Based on these reports, we determined whether PG could activate MAPKs in hAMSCs. In serum starvation condition, PG (10 M) induced ERK1/2 and p38 phosphorylation, but not JNK phosphorylation (Fig. 4A). In addition, treatment with PG (10 M) potentiated ERK1/2 and p38 phosphorylation under AIM conditions compared to treatment with vehicle control (Figs. 4B and 4C).

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