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Effect of Glucagon-like Peptide-1 on the Differentiation of Adipose-derived Stem Cells into Osteoblasts and Adipocytes.

Lee HM, Joo BS, Lee CH, Kim HY, Ock JH, Lee YS - J Menopausal Med (2015)

Bottom Line: In contrast, GLP-1 significantly suppressed the expression of adipocyte-specific markers, peroxisome proliferator-activated receptor gamma (PPAR-γ), lipoprotein lipase (LPL) and adipocyte protein 2 (AP2).This decreased expression of adipocyte specific markers caused by GLP-1 was significantly reversed by the treatment of extracellular signal-regulated kinase (ERK) inhibitor, PD98059 (P < 0.05).This result demonstrates that GLP-1 stimulates osteoblast differentiation in ADSCs, whereas it inhibits adipocyte differentiation.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Natural Science College, Pusan National University, Busan, Korea.

ABSTRACT

Objectives: Glucagon-like peptide-1 (GLP-1) is an intestinally secreted hormone and it plays an important role in the regulation of glucose homeostasis. However, the possible role of GLP-1 in the differentiation of adipose-derived stem cells (ADSCs) remains unknown. Therefore this study investigated the effect of GLP-1 on the differentiation of ADSCs into osteoblasts and adipocytes.

Methods: ADSCs were isolated from human adipose tissues of the abdomens, cultured and characterized by flow cytometry and multi-lineage potential assay. ADSCs were induced in osteogenic and adipogenic media treated with two different doses (10 and 100 nM) of GLP-1, and then the effect of GLP-1 on differentiation of ADSCs into osteoblast and adipocyte was examined. The signaling pathway involved in these processes was also examined.

Results: Isolated human ADSCs expressed mesenchymal stem cell (MSC) specific markers as well as GLP-1 receptor (GLP-1R) proteins. They also showed multiple-lineage potential of MSC. GLP-1 was upregulated the activity and mRNA expression of osteoblast-specific marker, alkaline phosphatase and the mineralization of calcium. In contrast, GLP-1 significantly suppressed the expression of adipocyte-specific markers, peroxisome proliferator-activated receptor gamma (PPAR-γ), lipoprotein lipase (LPL) and adipocyte protein 2 (AP2). This decreased expression of adipocyte specific markers caused by GLP-1 was significantly reversed by the treatment of extracellular signal-regulated kinase (ERK) inhibitor, PD98059 (P < 0.05).

Conclusion: This result demonstrates that GLP-1 stimulates osteoblast differentiation in ADSCs, whereas it inhibits adipocyte differentiation. The ERK signaling pathway seems to be involved in these differentiation processes mediated by GLP-1.

No MeSH data available.


Related in: MedlinePlus

The treatment of extracellular signal-regulated kinase (ERK) inhibitor in adipogenic differentiation of adipose-derived stem cells (ADSCs) by glucagon-like peptide-1 (GLP-1). ADSCs were induced with adipogenic induction medium (AIM) for 7 days in the presence or absence of GLP-1 and then they were treated with ERK inhibitor PD98059. Real time polymerase chain reaction (PCR) for indicated genes were performed. *P < 0.05 (vs. GLP-1(+) / PD98059(-) group).
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Figure 5: The treatment of extracellular signal-regulated kinase (ERK) inhibitor in adipogenic differentiation of adipose-derived stem cells (ADSCs) by glucagon-like peptide-1 (GLP-1). ADSCs were induced with adipogenic induction medium (AIM) for 7 days in the presence or absence of GLP-1 and then they were treated with ERK inhibitor PD98059. Real time polymerase chain reaction (PCR) for indicated genes were performed. *P < 0.05 (vs. GLP-1(+) / PD98059(-) group).

Mentions: To understand the signaling pathway involved in the inhibitory effect of GLP-1 on the adipocyte differentiation of ADSCs, ADSCs cultured in AIM in the presence or absence of GLP-1 were treated with ERK inhibitor, PD98059. GLP-1 treatment decreased expression of PPAR-γ, LPL and AP2 mRNA levels and this decreased effect caused by GLP-1 was significantly reversed by the treatment of ERK inhibitor (P < 0.05) (Fig. 5).


Effect of Glucagon-like Peptide-1 on the Differentiation of Adipose-derived Stem Cells into Osteoblasts and Adipocytes.

Lee HM, Joo BS, Lee CH, Kim HY, Ock JH, Lee YS - J Menopausal Med (2015)

The treatment of extracellular signal-regulated kinase (ERK) inhibitor in adipogenic differentiation of adipose-derived stem cells (ADSCs) by glucagon-like peptide-1 (GLP-1). ADSCs were induced with adipogenic induction medium (AIM) for 7 days in the presence or absence of GLP-1 and then they were treated with ERK inhibitor PD98059. Real time polymerase chain reaction (PCR) for indicated genes were performed. *P < 0.05 (vs. GLP-1(+) / PD98059(-) group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4561747&req=5

Figure 5: The treatment of extracellular signal-regulated kinase (ERK) inhibitor in adipogenic differentiation of adipose-derived stem cells (ADSCs) by glucagon-like peptide-1 (GLP-1). ADSCs were induced with adipogenic induction medium (AIM) for 7 days in the presence or absence of GLP-1 and then they were treated with ERK inhibitor PD98059. Real time polymerase chain reaction (PCR) for indicated genes were performed. *P < 0.05 (vs. GLP-1(+) / PD98059(-) group).
Mentions: To understand the signaling pathway involved in the inhibitory effect of GLP-1 on the adipocyte differentiation of ADSCs, ADSCs cultured in AIM in the presence or absence of GLP-1 were treated with ERK inhibitor, PD98059. GLP-1 treatment decreased expression of PPAR-γ, LPL and AP2 mRNA levels and this decreased effect caused by GLP-1 was significantly reversed by the treatment of ERK inhibitor (P < 0.05) (Fig. 5).

Bottom Line: In contrast, GLP-1 significantly suppressed the expression of adipocyte-specific markers, peroxisome proliferator-activated receptor gamma (PPAR-γ), lipoprotein lipase (LPL) and adipocyte protein 2 (AP2).This decreased expression of adipocyte specific markers caused by GLP-1 was significantly reversed by the treatment of extracellular signal-regulated kinase (ERK) inhibitor, PD98059 (P < 0.05).This result demonstrates that GLP-1 stimulates osteoblast differentiation in ADSCs, whereas it inhibits adipocyte differentiation.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Natural Science College, Pusan National University, Busan, Korea.

ABSTRACT

Objectives: Glucagon-like peptide-1 (GLP-1) is an intestinally secreted hormone and it plays an important role in the regulation of glucose homeostasis. However, the possible role of GLP-1 in the differentiation of adipose-derived stem cells (ADSCs) remains unknown. Therefore this study investigated the effect of GLP-1 on the differentiation of ADSCs into osteoblasts and adipocytes.

Methods: ADSCs were isolated from human adipose tissues of the abdomens, cultured and characterized by flow cytometry and multi-lineage potential assay. ADSCs were induced in osteogenic and adipogenic media treated with two different doses (10 and 100 nM) of GLP-1, and then the effect of GLP-1 on differentiation of ADSCs into osteoblast and adipocyte was examined. The signaling pathway involved in these processes was also examined.

Results: Isolated human ADSCs expressed mesenchymal stem cell (MSC) specific markers as well as GLP-1 receptor (GLP-1R) proteins. They also showed multiple-lineage potential of MSC. GLP-1 was upregulated the activity and mRNA expression of osteoblast-specific marker, alkaline phosphatase and the mineralization of calcium. In contrast, GLP-1 significantly suppressed the expression of adipocyte-specific markers, peroxisome proliferator-activated receptor gamma (PPAR-γ), lipoprotein lipase (LPL) and adipocyte protein 2 (AP2). This decreased expression of adipocyte specific markers caused by GLP-1 was significantly reversed by the treatment of extracellular signal-regulated kinase (ERK) inhibitor, PD98059 (P < 0.05).

Conclusion: This result demonstrates that GLP-1 stimulates osteoblast differentiation in ADSCs, whereas it inhibits adipocyte differentiation. The ERK signaling pathway seems to be involved in these differentiation processes mediated by GLP-1.

No MeSH data available.


Related in: MedlinePlus