Mechanical strain downregulates C/EBPβ in MSC and decreases endoplasmic reticulum stress

Mechanical strain downregulates C/EBPβ in MSC and decreases endoplasmic reticulum stress

Exercise prevents marrow mesenchymal stem cell (MSC) adipogenesis, reversing trends that accompany aging and osteoporosis. Mechanical input, the in-vitro analogue to exercise, limits PPARγ expression and adipogenesis in MSC. We considered whether C/EBPβ might be mechanoresponsive as it is upstream t...

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Veröffentlicht in:PloS one 2012-12, Vol.7 (12), p.e51613
Hauptverfasser: Styner, Maya, Meyer, Mark B, Galior, Kornelia, Case, Natasha, Xie, Zhihui, Sen, Buer, Thompson, William R, Pike, John Wesley, Rubin, Janet
Format: Artikel
Sprache:eng
Schlagworte:
Adipogenesis
Aging
Animals
Apoptosis
Biochemistry
Biocompatibility
Biology
Biomedical materials
CCAAT-Enhancer-Binding Protein-beta - genetics
CHOP protein
Down-Regulation - drug effects
Endocrinology
Endoplasmic reticulum
Endoplasmic Reticulum Stress - drug effects
Experiments
Gene expression
Gene silencing
Inhibition
Insulin
Kinases
Mechanical control
Mechanical stimuli
Medicine
Mesenchymal stem cells
Mesenchymal Stem Cells - drug effects
Mesenchymal Stem Cells - metabolism
Mesenchyme
Mice
Mice, Inbred C57BL
Osteoporosis
Pluripotency
Protein folding
Proteins
siRNA
Stem cells
Strain
Stress
Stress, Mechanical
Stresses
Tunicamycin
Tunicamycin - pharmacology
β-Catenin
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Zusammenfassung:Exercise prevents marrow mesenchymal stem cell (MSC) adipogenesis, reversing trends that accompany aging and osteoporosis. Mechanical input, the in-vitro analogue to exercise, limits PPARγ expression and adipogenesis in MSC. We considered whether C/EBPβ might be mechanoresponsive as it is upstream to PPARγ, and also is known to upregulate endoplasmic reticulum (ER) stress. MSC (C3H10T1/2 pluripotent cells as well as mouse marrow-derived MSC) were cultured in adipogenic media and a daily mechanical strain regimen was applied. We demonstrate herein that mechanical strain represses C/EBPβ mRNA (0.6-fold ±0.07, p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0051613