Periprosthetic strain magnitude-dependent upregulation of type I collagen synthesis in human osteoblasts through an ERK1/2 pathway

Department of Orthopaedics, Shanghai 6th People's Hospital, Shanghai Jiaotong University, 600 Yishan Road, Shanghai, 200233, China.
International Orthopaedics (Impact Factor: 2.11). 03/2009; 33(5):1455-60. DOI: 10.1007/s00264-009-0735-z
Source: PubMed

ABSTRACT Human osteoblasts sense mechanical stimulation and synthesise type I collagen in periprosthetic osseointegration following total hip arthroplasty. However, the regulation of type I collagen synthesis by periprosthetic strain is unclear because the cellular-level strain magnitude remains unknown to date. Fortunately, the tissue-level strain in implanted femurs is measurable. According to the mechanism of strain amplification, the tissue-level strain was amplified 20 times to stretch human osteoblasts in this study. Elongation of 0.8-3.2% enhanced the mRNA level of type I collagen, whereas the release of procollagen type I C propeptide only increased at 2.4% and 3.2% elongation. Type I collagen expression increased with the activation of ERK1/2 phosphorylation in a strain-magnitude-dependent manner, whereas JNK and P38 were unaffected. The responses were completely inhibited by blocking the ERK1/2 pathway with U0126. The results indicate that type I collagen synthesis in human osteoblasts depends on the level of periprosthetic strain and ERK1/2 activation.

6 Reads
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this paper, we present two specifications, scalable DEVS specification and distributed container object specification, to support scalability and interoperability of DEVS-based modeling and simulation (M and S) systems. The scalable DEVS specification lists a set of interfaces which create and simulate DEVS models, and control simulation activities among simulators. The distributed container object specification provides a heterogeneous and distributed collection framework focusing on ensemble operations. The proposed specifications contain a rich set of both data and operations which are necessary for building scalable M and S environments that should provide invariance in both performance and quality of service of a system as the size, complexity, and interdependence of its elements increases. We describe design and implementation aspects of those specifications
    Systems, Man, and Cybernetics, 2001 IEEE International Conference on; 02/2001
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Nuclear factor kappa B (NF-κB) plays a prominent role in the pathogenesis of infectious diseases. Staphylococcus aureus (S. aureus), which can attach to and invade human osteoblasts, is the most common causative agent of osteomyelitis. To determine whether S. aureus can activate NF-κB in human osteoblasts and explore the possible factors of activation in response to infection, we used flow cytometry, enzyme-linked immunosorbent assay, immunoblots, and electrophoretic mobility shift assays to quantify the invasion of bacteria, to measure the interleukin-6 (IL-6) of culture supernatants, and to investigate the IκBα degradation and NF-κB activation in human osteoblasts. Moreover, we explored the possible factors responsible for the activation of NF-κB by preventing S. aureus from physically touching human osteoblasts or inhibiting the invasion of S. aureus into human osteoblasts under co-culture conditions, by incubating proteinase K-treated or ultraviolet-killed S. aureus with human osteoblasts and by treating human osteoblasts with peptidoglycan (PGN) or lipoteichoic acid (LTA). We found that S. aureus induced the IκBα degradation and NF-κB activation, which could regulate IL-6 secretion in the culture supernatants of human osteoblasts in response to infection. In addition, the maximal IκBα degradation and NF-κB activation in human osteoblasts occurred prior to the maximal invasion of S. aureus. It was the attachment not invasion or the secreted soluble factor(s), PGN, LTA of S. aureus, that could induce the IκBα degradation and NF-κB activation in human osteoblasts. These results indicated that S. aureus can activate NF-κB in human osteoblasts and that the attachment of S. aureus is required for this activation in response to infection.
    Acta Biochimica et Biophysica Sinica 11/2010; 42(12):883-92. DOI:10.1093/abbs/gmq096 · 2.19 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Activation of nuclear factor kappaB by diverse bacteria regulates the secretion of chemokines and cytokines. Staphylococcus aureus (S. aureus)-infected osteoblasts can significantly increase the secretion of interleukin-6 and monocyte chemoattractant protein-1. The aim of this study was to investigate whether S. aureus can activate nuclear factor kappaB in human osteoblasts, and whether the activation of nuclear factor kappaB by S. aureus regulates the secretion of interleukin-6 and monocyte chemoattractant protein-1.
    The Brazilian journal of infectious diseases: an official publication of the Brazilian Society of Infectious Diseases 06/2011; 15(3):189-94. DOI:10.1016/S1413-8670(11)70173-8 · 1.30 Impact Factor
Show more


6 Reads
Available from