Cyclic tensile stress promotes osteogenic differentiation of adipose stem cells via ERK and p38 pathways.

Cyclic tensile stress promotes osteogenic differentiation of adipose stem cells via ERK and p38... The present study aimed to elucidate whether extracellular signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen-activated protein kinases pathways participate in the transduction of mechanical stretch exerted on adipose stem cells (ASCs) into intracellular osteogenic signals, and if so whether both pathways have time-dependent feature. Rat ASCs were cultured in osteogenic medium for 72 h and assigned into three sets, namely ERK1/2 inhibitor treated set, p38 inhibitor treated set, and the control set. After inhibitor treatment, all cells were subjected to cyclic stretch(2000 με, 1 Hz) on a four-point bending mechanical loading device. Protein and mRNA samples were acquired at six time points: 0, 15 min, 30 min, 1 h, 2 h and 6 h. Western blot showed phosphorylation level of ERK1/2 was elevated by cyclic tensile stress at all time points, while p38 at 15 min, 30 min and 1 h, and the elevation can be completely blocked by corresponding inhibitors. The treatment by ERK1/2 inhibitor was shown to antagonize the up-regulation of osteogenic genes bone morphogenetic protein 2 (BMP-2) and runt-related transcription factor 2 (Runx2) by mechanical stretch at 15 min and 6 h, whereas p38 inhibitor took effect at 15 min only. The results suggested both ERK and p38 could be positive mediators of stretch-induced osteogenic differentiation of ASCs, and ERK stimulate the stretch-induced osteogenic differentiation at both early and late stages while p38 responds to mechanical stretch in a more rapid fashion. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Stem cell research Pubmed

Cyclic tensile stress promotes osteogenic differentiation of adipose stem cells via ERK and p38 pathways.

Stem cell research, Volume 37: 1 – Oct 21, 2019
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Cyclic tensile stress promotes osteogenic differentiation of adipose stem cells via ERK and p38 pathways.

Stem cell research, Volume 37: 1 – Oct 21, 2019

Abstract

The present study aimed to elucidate whether extracellular signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen-activated protein kinases pathways participate in the transduction of mechanical stretch exerted on adipose stem cells (ASCs) into intracellular osteogenic signals, and if so whether both pathways have time-dependent feature. Rat ASCs were cultured in osteogenic medium for 72 h and assigned into three sets, namely ERK1/2 inhibitor treated set, p38 inhibitor treated set, and the control set. After inhibitor treatment, all cells were subjected to cyclic stretch(2000 με, 1 Hz) on a four-point bending mechanical loading device. Protein and mRNA samples were acquired at six time points: 0, 15 min, 30 min, 1 h, 2 h and 6 h. Western blot showed phosphorylation level of ERK1/2 was elevated by cyclic tensile stress at all time points, while p38 at 15 min, 30 min and 1 h, and the elevation can be completely blocked by corresponding inhibitors. The treatment by ERK1/2 inhibitor was shown to antagonize the up-regulation of osteogenic genes bone morphogenetic protein 2 (BMP-2) and runt-related transcription factor 2 (Runx2) by mechanical stretch at 15 min and 6 h, whereas p38 inhibitor took effect at 15 min only. The results suggested both ERK and p38 could be positive mediators of stretch-induced osteogenic differentiation of ASCs, and ERK stimulate the stretch-induced osteogenic differentiation at both early and late stages while p38 responds to mechanical stretch in a more rapid fashion.
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DOI
10.1016/j.scr.2019.101433

Abstract

The present study aimed to elucidate whether extracellular signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen-activated protein kinases pathways participate in the transduction of mechanical stretch exerted on adipose stem cells (ASCs) into intracellular osteogenic signals, and if so whether both pathways have time-dependent feature. Rat ASCs were cultured in osteogenic medium for 72 h and assigned into three sets, namely ERK1/2 inhibitor treated set, p38 inhibitor treated set, and the control set. After inhibitor treatment, all cells were subjected to cyclic stretch(2000 με, 1 Hz) on a four-point bending mechanical loading device. Protein and mRNA samples were acquired at six time points: 0, 15 min, 30 min, 1 h, 2 h and 6 h. Western blot showed phosphorylation level of ERK1/2 was elevated by cyclic tensile stress at all time points, while p38 at 15 min, 30 min and 1 h, and the elevation can be completely blocked by corresponding inhibitors. The treatment by ERK1/2 inhibitor was shown to antagonize the up-regulation of osteogenic genes bone morphogenetic protein 2 (BMP-2) and runt-related transcription factor 2 (Runx2) by mechanical stretch at 15 min and 6 h, whereas p38 inhibitor took effect at 15 min only. The results suggested both ERK and p38 could be positive mediators of stretch-induced osteogenic differentiation of ASCs, and ERK stimulate the stretch-induced osteogenic differentiation at both early and late stages while p38 responds to mechanical stretch in a more rapid fashion.

Journal

Stem cell researchPubmed

Published: Oct 21, 2019

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