Inhibition of adipogenic differentiation of bone marrow mesenchymal stem cells by erythropoietin via activating ERK and P38 MAPK

Liu, G X; Zhu, Jingjie; Chen, X Y; Zhu, Aizhen; Liu, C C; Lai, Qun; Chen, S T

doi:10.4238/2015.june.26.5

Cited by 15 publications

(8 citation statements)

References 19 publications

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“…Despite the negative impact that this cell population may have on bone formation in contact with Ti implant , the effect of Ti surfaces on adipocyte differentiation and/or activity is underexplored, making comparisons of these results with data from the literature difficult or even unfeasible. However, our findings are in agreement, to some extent, with the reduced ERK activity detected during adipogenesis in cultures of the ST2 mouse MSC line, the increased ERK phosphorylation associated with reduced adipocyte differentiation of mouse MSCs, and recovery of the propyl gallate‐inhibiting adipogenic potential of human MSCs in response to ERK blocking .…”

Section: Discussionsupporting

confidence: 89%

Participation of extracellular signal‐regulated kinases 1/2 in osteoblast and adipocyte differentiation of mesenchymal stem cells grown on titanium surfaces

Silva

Abuna

Lopes

et al. 2017

European J Oral Sciences

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Osteoblasts and adipocytes coexist in the implantation site and affect the process of titanium (Ti) osseointegration. As extracellular signal-regulated kinases 1/2 (ERK1/2) are involved in osteogenesis and adipogenesis, the aim of our study was to investigate if the effects of Ti surface topography on osteoblast and adipocyte differentiation are modulated by ERK1/2. The experiments were conducted based on the effect of the ERK1/2 inhibitor, PD98059, on mesenchymal stem cells (MSCs) grown under osteogenic and adipogenic conditions on Ti with nanotopography (Ti-Nano) or on machined Ti (Ti-Machined). The results showed that, in general, ERK1/2 inhibition favored osteoblast and adipocyte differentiation of MSCs grown on Ti-Machined. In MSCs grown on Ti-Nano, ERK1/2 inhibition upregulated the expression of alkaline phosphatase and osteocalcin and reduced extracellular matrix mineralization. In terms of adipocyte differentiation, ERK1/2 inhibition elicited similar MSC responses to Ti-Nano and Ti-Machined, upregulating gene expression of adipocyte markers without affecting lipid accumulation. Our results indicate that, under osteogenic and adipogenic conditions, the responses of MSCs to Ti surface topography in terms of osteogenesis and adipogenesis are dependent on ERK1/2. Thus, a precise modulation of ERK1/2 expression and activity induced by surface topography could be a good strategy to drive the process of implant osseointegration.

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Section: Discussionsupporting

confidence: 89%

Participation of extracellular signal‐regulated kinases 1/2 in osteoblast and adipocyte differentiation of mesenchymal stem cells grown on titanium surfaces

Silva

Abuna

Lopes

et al. 2017

European J Oral Sciences

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“…Moreover, there is data demonstrating that erythropoietin inhibits adipogenic differentiation of bone marrow derived mouse MSCs via activation of ERK (Liu et al 2015). Finally, an inhibitory role has been demonstrated for JNK in both adipogenesis and osteogenesis in human MSCs (Gu et al 2015;Tominaga et al 2005).…”

Section: Discussionmentioning

confidence: 98%

Elevated levels of the small GTPase Cdc42 induces senescence in male rat mesenchymal stem cells

et al. 2018

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Mesenchymal stem cells (MSCs) represent a promising cell source for cellular therapy and tissue engineering and are currently being tested in a number of clinical trials for various diseases. However, like other somatic cells, MSCs age, and this senescence is accompanied by a progressive decline in stem cell function. Several lines of evidence suggest a role for the Rho family GTPase Cdc42 activity in cellular senescence processes. In the present study, we have examined aging-associated Cdc42 activity in rat adipose-derived mesenchymal stem cells (ADMSCs) and the consequences of pharmacological inhibition of Cdc42 in ADMSCs from aged rats. We demonstrate that ADMSCs show a decreased rate of cell growth and a decreased ability to differentiate into chrodrogenic, osteogenic and adipogenic cell lineages as a function of rat age. This is accompanied with an increased staining for SA-β-Gal activity and increased levels of Cdc42 bound to GTP. Treatment of ADMSCs from 24-month old rats with three Cdc42 inhibitors significantly increased proliferation rates, decreased SA-β-Gal staining, and reduced Cdc42-GTP. The Cdc42 inhibitor CASIN increased adipogenic and osteogenic differentiation potential in ADMSCs from 24-month old rats, and decreased the levels of radical oxygen species (ROS), p16 levels, F-actin, and the activity of the ERK1/2 and JNK signaling pathways that were all elevated in these cells. These data suggest that ADMSCs show increased rates of senescence as rats age that appear to be due to elevated Cdc42 activity. Thus, Cdc42 plays important roles in MSC senescence and differentiation potential, and pharmacological reduction of Cdc42 activity can, at least partially, rejuvenate aged MSCs.

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“…The role of p38 MAPK in adipogenesis is still controversial. While some studies have demonstrated that activation of p38 MAPK promotes adipogenesis [ 38 , 39 , 40 ], opposite results have also been reported [ 41 , 42 ]. Studies by Engelman et al and Aouadi et al suggested that p38 MAPK activity may be required in the initial stage of adipogenesis, and that suppression of p38 MAPK may be necessary in the later stage of adipogenesis [ 43 , 44 ].…”

Section: Discussionmentioning

confidence: 99%

Phloretin Promotes Adipogenesis via Mitogen-Activated Protein Kinase Pathways in Mouse Marrow Stromal ST2 Cells

Takeno

Kanazawa

Notsu

et al. 2018

IJMS

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Phloretin, a glucose transporter (GLUT) inhibitor, has pleiotropic effects. The present study examined the effects of phloretin on the commitment of marrow stromal cells to adipocytes, using the mouse marrow stromal cell line ST2. Oil red O staining showed that treatment with phloretin 10–100 µM promoted lipid accumulation. Real-time PCR showed that phloretin significantly increased the expression of adipogenic markers, including PPARγ, C/EBPα, fatty acid synthase, fatty acid-binding protein 4, and adiponectin. Western blotting showed that phloretin inhibited ERK1/2 and JNK but activated p38 MAPK. Treatment with a MAPK/ERK kinase inhibitor and a JNK inhibitor enhanced adipogenesis, similar to phloretin. In contrast, a p38 MAPK inhibitor suppressed phloretin-induced adipogenesis. Although phloretin phosphorylated AMP-activated protein kinase (AMPK), co-incubation with an AMPK inhibitor did not block phloretin-induced adipogenesis. The 2-deoxyglucose colorimetric assay showed that phloretin and siRNA silencing of GLUT1 decreased glucose uptake. However, unlike phloretin treatment, GLUT1 silencing inhibited adipogenesis. In addition, phloretin enhanced adipogenesis in GLUT1 knocked-down cells. Taken together, phloretin induced adipogenesis of marrow stromal cells by inhibiting ERK1/2 and JNK and by activating p38 MAPK. The adipogenic effects of phloretin were independent of glucose uptake inhibition. Phloretin may affect energy metabolism by influencing adipogenesis and adiponectin expression.

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Inhibition of adipogenic differentiation of bone marrow mesenchymal stem cells by erythropoietin via activating ERK and P38 MAPK

Cited by 15 publications

References 19 publications

Participation of extracellular signal‐regulated kinases 1/2 in osteoblast and adipocyte differentiation of mesenchymal stem cells grown on titanium surfaces

Participation of extracellular signal‐regulated kinases 1/2 in osteoblast and adipocyte differentiation of mesenchymal stem cells grown on titanium surfaces

Elevated levels of the small GTPase Cdc42 induces senescence in male rat mesenchymal stem cells

Phloretin Promotes Adipogenesis via Mitogen-Activated Protein Kinase Pathways in Mouse Marrow Stromal ST2 Cells

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