Limits...
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) negatively regulates adipogenesis through ERK activation. (A) hAMSCs were pre-treated with vehicle or PD98059 for 1 h before the addition of AIM containing 10 μM PG. ERK1/2 phosphorylation was monitored by immunoblotting 30 min after PG treatment. hAMSCs were pre-treated with vehicle or SB203580 for 1 h before the addition of AIM containing 10 μM PG. p38 phosphorylation was monitored by immunoblotting 30 min after the PG treatment; (B) hAMSCs were cultured under adipogenic differentiation conditions with or without PG (10 μM). The effect of PD98059 or SB203580 was examined. Lipid accumulation was confirmed by Oil Red-O staining at 14 days after adipogenic induction. Values represent the mean ± SD; (C) The expression of adipogenic markers aP2 and adipsin was examined in PG-treated cells with or without treatment with PD98059; (D) aP2 protein levels in hAMSCs were examined at day 14 after adipogenic induction. The levels of aP2 were normalized to actin. hAMSCs: human adi-pose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium; ERK: extracellular regulated kinase.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4400308&req=5

f5-molce-38-4-336: Propyl gallate (PG) negatively regulates adipogenesis through ERK activation. (A) hAMSCs were pre-treated with vehicle or PD98059 for 1 h before the addition of AIM containing 10 μM PG. ERK1/2 phosphorylation was monitored by immunoblotting 30 min after PG treatment. hAMSCs were pre-treated with vehicle or SB203580 for 1 h before the addition of AIM containing 10 μM PG. p38 phosphorylation was monitored by immunoblotting 30 min after the PG treatment; (B) hAMSCs were cultured under adipogenic differentiation conditions with or without PG (10 μM). The effect of PD98059 or SB203580 was examined. Lipid accumulation was confirmed by Oil Red-O staining at 14 days after adipogenic induction. Values represent the mean ± SD; (C) The expression of adipogenic markers aP2 and adipsin was examined in PG-treated cells with or without treatment with PD98059; (D) aP2 protein levels in hAMSCs were examined at day 14 after adipogenic induction. The levels of aP2 were normalized to actin. hAMSCs: human adi-pose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium; ERK: extracellular regulated kinase.

Mentions: To determine whether PG could inhibit adipogenesis via the ERK or p38 signaling pathway, we used the specific mitogen-activated protein kinase (MEK) inhibitor PD98059 to inhibit ERK phosphorylation. MEK is an upstream kinase of ERK. ERK activation can be prevented by blocking MEK activity(Crews et al., 1992). SB203580 was used to prevent p38 activation. PG-induced ERK1/2 and p38 phosphorylation was significantly (p < 0.05) inhibited in response to treatment by each inhibitor (Fig. 5A). Treatment of PD98059 recovered PG-mediated inhibition of lipid accumulation in a dose-dependent manner (Fig. 5B), indicating that PG prevented adipogenic differentiation of hAMSCs via the ERK pathway. The absorbance of extracted Oil Red-O in the presence of PD98059 (20 μM) recovered to 77% of that found under normal differentiating conditions (Fig. 5B). In contrast, inhibiting the p38 signal pathway with the specific inhibitor SB203580 did not affect PG anti-adipogenic activity (Fig. 5B). Additionally, expressions of the adipocyte specific protein aP2 and adipsin were rescued in a dose dependent manner by inhibiting ERK (Fig. 5C). Our data clearly show that the ERK signaling pathway is required for anti-adipogenic activity of PG. Taken together, these results suggest that PG inhibits adipogenesis possibly via sustained activation of ERK without depending on the activation of other MAPKs.


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) negatively regulates adipogenesis through ERK activation. (A) hAMSCs were pre-treated with vehicle or PD98059 for 1 h before the addition of AIM containing 10 μM PG. ERK1/2 phosphorylation was monitored by immunoblotting 30 min after PG treatment. hAMSCs were pre-treated with vehicle or SB203580 for 1 h before the addition of AIM containing 10 μM PG. p38 phosphorylation was monitored by immunoblotting 30 min after the PG treatment; (B) hAMSCs were cultured under adipogenic differentiation conditions with or without PG (10 μM). The effect of PD98059 or SB203580 was examined. Lipid accumulation was confirmed by Oil Red-O staining at 14 days after adipogenic induction. Values represent the mean ± SD; (C) The expression of adipogenic markers aP2 and adipsin was examined in PG-treated cells with or without treatment with PD98059; (D) aP2 protein levels in hAMSCs were examined at day 14 after adipogenic induction. The levels of aP2 were normalized to actin. hAMSCs: human adi-pose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium; ERK: extracellular regulated kinase.
© Copyright Policy
Related In: Results  -  Collection

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

f5-molce-38-4-336: Propyl gallate (PG) negatively regulates adipogenesis through ERK activation. (A) hAMSCs were pre-treated with vehicle or PD98059 for 1 h before the addition of AIM containing 10 μM PG. ERK1/2 phosphorylation was monitored by immunoblotting 30 min after PG treatment. hAMSCs were pre-treated with vehicle or SB203580 for 1 h before the addition of AIM containing 10 μM PG. p38 phosphorylation was monitored by immunoblotting 30 min after the PG treatment; (B) hAMSCs were cultured under adipogenic differentiation conditions with or without PG (10 μM). The effect of PD98059 or SB203580 was examined. Lipid accumulation was confirmed by Oil Red-O staining at 14 days after adipogenic induction. Values represent the mean ± SD; (C) The expression of adipogenic markers aP2 and adipsin was examined in PG-treated cells with or without treatment with PD98059; (D) aP2 protein levels in hAMSCs were examined at day 14 after adipogenic induction. The levels of aP2 were normalized to actin. hAMSCs: human adi-pose tissue-derived mesenchymal stem cells; AIM: adipogenic induction medium; ERK: extracellular regulated kinase.
Mentions: To determine whether PG could inhibit adipogenesis via the ERK or p38 signaling pathway, we used the specific mitogen-activated protein kinase (MEK) inhibitor PD98059 to inhibit ERK phosphorylation. MEK is an upstream kinase of ERK. ERK activation can be prevented by blocking MEK activity(Crews et al., 1992). SB203580 was used to prevent p38 activation. PG-induced ERK1/2 and p38 phosphorylation was significantly (p < 0.05) inhibited in response to treatment by each inhibitor (Fig. 5A). Treatment of PD98059 recovered PG-mediated inhibition of lipid accumulation in a dose-dependent manner (Fig. 5B), indicating that PG prevented adipogenic differentiation of hAMSCs via the ERK pathway. The absorbance of extracted Oil Red-O in the presence of PD98059 (20 μM) recovered to 77% of that found under normal differentiating conditions (Fig. 5B). In contrast, inhibiting the p38 signal pathway with the specific inhibitor SB203580 did not affect PG anti-adipogenic activity (Fig. 5B). Additionally, expressions of the adipocyte specific protein aP2 and adipsin were rescued in a dose dependent manner by inhibiting ERK (Fig. 5C). Our data clearly show that the ERK signaling pathway is required for anti-adipogenic activity of PG. Taken together, these results suggest that PG inhibits adipogenesis possibly via sustained activation of ERK without depending on the activation of other MAPKs.

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