Abstract
Recent findings support the idea that fluid movement in the bone is a key factor in bone formation and related cellular responses. However, the precise molecular mechanisms are not known. Our data demonstrates that fluid shear stress is a key factor in the activation of specific transcriptional pathways in murine preosteoblast (MC3T3E1) cells. MC3T3E1 cells have increased expression of the egr-1 and p57kip2 genes after being subjected to 0.3 dynes/cm2 of fluid shear stress. The MC3T3E1 cells are already known to express egr-1, a multipotent transcription factor, after high levels of fluid shear stress, but this is the first demonstration of egr-1 expression after low levels of fluid shear stress. Moreover, this is the first study showing expression of p57kip2 by the MC3T3E1 cells after fluid shear stress. The expression of p57kip2, a cyclin dependent kinase inhibitor, is a strong indicator that the cells are exiting the cell cycle and are beginning to differentiate. Our data shows decreased 3H-thymidine incorporation up to 18 hours post stress, which agrees with the upregulation of p57kip2 as a result of fluid shear stress.
Original language | English (US) |
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Pages (from-to) | 1-6 |
Number of pages | 6 |
Journal | Biomedical Sciences Instrumentation |
Volume | 37 |
State | Published - 2001 |
Externally published | Yes |
Keywords
- Egr-1
- MC3T3E1
- Macroarray
- Preosteoblast
- Shear stress
- p57kip2
ASJC Scopus subject areas
- Biophysics
- Medical Laboratory Technology