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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) decreases mRNA and protein level of adipocyte-specific markers. (A) hAMSCs were cultured in AIM with or without 10 μM PG. Gene expression of C/EBP-α, PPAR-γ, LPL, aP2, and adiponectin was examined by real-time PCR. The mean values obtained from vehicle-treated cells at 0 day were considered as 1.0. Others were relative values. Values are presented as mean ± SD. Error bars indicate results range for treatment performed in triplicates. *p < 0.05 compared to control. Results are representative of two independent experiments; (B) PG decreases expression of adipocyte-specific marker proteins. Protein levels of adipogenic markers were examined during adipogenesis. Results are representative of three independent experiments. aP2: adipocyte fatty acid-binding protein; C/EBP-α: CCAAT enhancer binding protein-α LPL, lipoprotein lipase; PCR: polymerase chain reaction; PPAR-γ: peroxisome proliferator-activated receptor-γ.
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f2-molce-38-4-336: Propyl gallate (PG) decreases mRNA and protein level of adipocyte-specific markers. (A) hAMSCs were cultured in AIM with or without 10 μM PG. Gene expression of C/EBP-α, PPAR-γ, LPL, aP2, and adiponectin was examined by real-time PCR. The mean values obtained from vehicle-treated cells at 0 day were considered as 1.0. Others were relative values. Values are presented as mean ± SD. Error bars indicate results range for treatment performed in triplicates. *p < 0.05 compared to control. Results are representative of two independent experiments; (B) PG decreases expression of adipocyte-specific marker proteins. Protein levels of adipogenic markers were examined during adipogenesis. Results are representative of three independent experiments. aP2: adipocyte fatty acid-binding protein; C/EBP-α: CCAAT enhancer binding protein-α LPL, lipoprotein lipase; PCR: polymerase chain reaction; PPAR-γ: peroxisome proliferator-activated receptor-γ.

Mentions: Adipocyte differentiation is accompanied by altered expression of various transcription factors and adipocyte-specific genes (Sermeus et al., 2008). To further confirm the effect of PG on adipocyte differentiation, we performed real-time PCR to determine the expression of PPAR-γ and C/EBP-α, two key transcriptional factors involved in adipogenesis. We also checked the mRNA expression levels of aP2, adiponectin, and LPL. The mRNA expression levels of PPAR-γ, C/EBP-α, LPL, aP2, and adiponectin were significantly (p < 0.05) decreased following treatment with 10 μM PG (Fig. 2A). At 6 days after PG treatment, the mRNA expression levels of both PPAR-γ and C/EBP-α expressions were significantly (p < 0.05) inhibited. The transcriptional levels of aP2, adiponectin, and LPL were also significantly (p < 0.05) inhibited by PG treatment. In addition, the protein levels of adipocyte-specific markers were significantly (p < 0.05) decreased following PG treatment under adipogenic differentiation conditions (Fig. 2B). These results suggest that PG can inhibit adipocyte differentiation of hAMSCs.


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) decreases mRNA and protein level of adipocyte-specific markers. (A) hAMSCs were cultured in AIM with or without 10 μM PG. Gene expression of C/EBP-α, PPAR-γ, LPL, aP2, and adiponectin was examined by real-time PCR. The mean values obtained from vehicle-treated cells at 0 day were considered as 1.0. Others were relative values. Values are presented as mean ± SD. Error bars indicate results range for treatment performed in triplicates. *p < 0.05 compared to control. Results are representative of two independent experiments; (B) PG decreases expression of adipocyte-specific marker proteins. Protein levels of adipogenic markers were examined during adipogenesis. Results are representative of three independent experiments. aP2: adipocyte fatty acid-binding protein; C/EBP-α: CCAAT enhancer binding protein-α LPL, lipoprotein lipase; PCR: polymerase chain reaction; PPAR-γ: peroxisome proliferator-activated receptor-γ.
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f2-molce-38-4-336: Propyl gallate (PG) decreases mRNA and protein level of adipocyte-specific markers. (A) hAMSCs were cultured in AIM with or without 10 μM PG. Gene expression of C/EBP-α, PPAR-γ, LPL, aP2, and adiponectin was examined by real-time PCR. The mean values obtained from vehicle-treated cells at 0 day were considered as 1.0. Others were relative values. Values are presented as mean ± SD. Error bars indicate results range for treatment performed in triplicates. *p < 0.05 compared to control. Results are representative of two independent experiments; (B) PG decreases expression of adipocyte-specific marker proteins. Protein levels of adipogenic markers were examined during adipogenesis. Results are representative of three independent experiments. aP2: adipocyte fatty acid-binding protein; C/EBP-α: CCAAT enhancer binding protein-α LPL, lipoprotein lipase; PCR: polymerase chain reaction; PPAR-γ: peroxisome proliferator-activated receptor-γ.
Mentions: Adipocyte differentiation is accompanied by altered expression of various transcription factors and adipocyte-specific genes (Sermeus et al., 2008). To further confirm the effect of PG on adipocyte differentiation, we performed real-time PCR to determine the expression of PPAR-γ and C/EBP-α, two key transcriptional factors involved in adipogenesis. We also checked the mRNA expression levels of aP2, adiponectin, and LPL. The mRNA expression levels of PPAR-γ, C/EBP-α, LPL, aP2, and adiponectin were significantly (p < 0.05) decreased following treatment with 10 μM PG (Fig. 2A). At 6 days after PG treatment, the mRNA expression levels of both PPAR-γ and C/EBP-α expressions were significantly (p < 0.05) inhibited. The transcriptional levels of aP2, adiponectin, and LPL were also significantly (p < 0.05) inhibited by PG treatment. In addition, the protein levels of adipocyte-specific markers were significantly (p < 0.05) decreased following PG treatment under adipogenic differentiation conditions (Fig. 2B). These results suggest that PG can inhibit adipocyte differentiation of hAMSCs.

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