Biochemical signal transduction of mechanical strain in osteoblast-like cells

Jones, David B.; Nolte, Hendrik; Scholübbers, J G; Turner, Emma M.; Veltel, D

doi:10.1016/0142-9612(91)90186-e

Cited by 257 publications

(139 citation statements)

References 35 publications

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“…This idea has yet to be proved experimentally, and in the future such relationships will need to be more accurately defined from in vitro experiments such as those of Jones et al (1991) The axi-symmetric finite element model of the knee, as well as the linear poroelastic constitutive models of the tissues, are simplifications of a complex biomechanical system. The fluid boundary conditions at the cartilage surfaces are also extremely difficult to quantify.…”

Section: Discussionmentioning

confidence: 99%

“…Inter-patient variation has also been observed (Fermor et al, 1998). Jones et al (1991) compared the mitosis rates of two types of osteoblastlike cells and skin fibroblasts to different magnitudes of strain. Only under the application of large strains (10,000 µstrains) was an increase in mitosis observed in all cell types, however these large strains were seen to cause de-differentiation of the osteoblasts into a fibroblast-like cell.…”

Section: Implementation Of the Mechano-regulation Algorithmmentioning

confidence: 99%

“…Cell mitosis has been shown to depend on the cell type (Jones et al, 1991) and the origin of the cell within the body (Brighton et al, 1991), as well as magnitude (Jones et al, 1991), frequency and number of cycles (Kasper et al, 2002) of the applied strain. Inter-patient variation has also been observed (Fermor et al, 1998).…”

Section: Implementation Of the Mechano-regulation Algorithmmentioning

confidence: 99%

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Mechano-regulation of stem cell differentiation and tissue regeneration in osteochondral defects

Kelly

Prendergast

2005

Journal of Biomechanics

184

134

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Cartilage defects that penetrate the subchondral bone can undergo spontaneous repair through the formation of a fibrous or cartilaginous tissue mediated primarily by mesenchymal stem cells from the bone marrow. This tissue is biomechanically inferior to normal articular cartilage, and is often observed to degrade over time. The factors that control the type and quality of the repair tissue, and its subsequent degradation, have yet to be elucidated. In this paper, we hypothesise a relationship between the mechanical environment of mesenchymal stem cells and their subsequent dispersal, proliferation, differentiation and death. The mechano-regulation stimulus is hypothesised to be a function of strain and fluid flow; these quantities are calculated using a finite element model of the tissue. A finite element model of an osteochondral defect in the knee was created, and used to simulate the spontaneous repair process.

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Section: Discussionmentioning

confidence: 99%

Section: Implementation Of the Mechano-regulation Algorithmmentioning

confidence: 99%

Section: Implementation Of the Mechano-regulation Algorithmmentioning

confidence: 99%

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Mechano-regulation of stem cell differentiation and tissue regeneration in osteochondral defects

Kelly

Prendergast

2005

Journal of Biomechanics

184

134

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“…Twenty percent of the femoral neck surface has cellular periosteum which suggests that anabolic osteogenic therapies may be effective in strengthening this clinically relevant site. Periosteal cells have greater sensitivity to mechanical 61 and pharmacological 82 stimuli compared to marrow cells and even limited cellular periosteum may be sufficient for enhancing periosteal apposition. These cells likely do serve to expand the periosteal diameter, as the femoral neck experiences age-associated radial expansion.…”

Section: Microscopic Featuresmentioning

confidence: 99%

RETRACTED: The periosteum

Augustin¹,

Antabak²,

Davila³

2007

Injury

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“…Such (re)-modeling requires bone resorption and deposition by the concerted efforts of osteoblasts and osteoclasts. Several studies have demonstrated that, in the absence of the systemic and local factors, mechanical loading on osteoblasts in vitro is able to increase prostaglandin release (4), stimulate cell division (5), alter collagen synthesis (6), and promote collagenase activity (7). Other induced proteins such as insulin-like growth factors I and II, transforming growth factor-␤, osteocalcin, osteopontin, nitric-oxide synthase, and cyclooxygease-2 have also been reported (8).…”

mentioning

confidence: 99%

Protein Kinase C-δ Transactivates Platelet-derived Growth Factor Receptor-α in Mechanical Strain-induced Collagenase 3 (Matrix Metalloproteinase-13) Expression by Osteoblast-like Cells

Yang

Hsieh

Yao

et al. 2009

Journal of Biological Chemistry

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Mechanical strain to bone is considered to be important for the maintenance of bone integrity and architecture. The process of bone (re)modeling under mechanical loading may repair fatigue damage and improve bone strength (1-3). Such (re)-modeling requires bone resorption and deposition by the concerted efforts of osteoblasts and osteoclasts. Several studies have demonstrated that, in the absence of the systemic and local factors, mechanical loading on osteoblasts in vitro is able to increase prostaglandin release (4), stimulate cell division (5), alter collagen synthesis (6), and promote collagenase activity (7). Other induced proteins such as insulin-like growth factors I and II, transforming growth factor-␤, osteocalcin, osteopontin, nitric-oxide synthase, and cyclooxygease-2 have also been reported (8).Previously, we reported that mechanical strain induces collagenase 3 (MMP-13) 2 expression by MC3T3-E1 osteoblastlike cells (9). The MMP-13 mRNA induction is transient, stable, and does not require de novo protein synthesis, suggesting that an immediate action be taken by strained osteoblasts to participate in the resorption phase of matrix (re)modeling. MMP-13 is a neutral proteinase capable of degrading native fibrillar collagens in the extracellular space (10, 11). It may be involved in situations where rapid and effective remodeling of collagenous extracellular matrix is required. Hence, MMP-13 can be detected in primary fetal ossification during bone morphogenesis, and in remodeling of the mature skeletal tissue (12,13).Mechanical strain induction of MMP-13 may be mediated through a process of mechanotransduction, converting physical forces into biochemical signals and integrating these signals into cellular responses. In our stretch chamber system, we showed that the mechanotransduction utilizes the MEK/ERK signaling pathway to implement MMP-13 expression (9). However, the transduction mechanism involved remains unclear and awaits further investigation. Three lines of studies have prompted us to investigate the receptor of platelet-derived growth factor receptor (PDGFR) as a potential mechanoreceptor in the MMP-13 induction. PDGF-BB induces MMP-13 expression in osteoblasts (14, 15), whereas in vascular smooth

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Biochemical signal transduction of mechanical strain in osteoblast-like cells

Cited by 257 publications

References 35 publications

Mechano-regulation of stem cell differentiation and tissue regeneration in osteochondral defects

Mechano-regulation of stem cell differentiation and tissue regeneration in osteochondral defects

RETRACTED: The periosteum

Protein Kinase C-δ Transactivates Platelet-derived Growth Factor Receptor-α in Mechanical Strain-induced Collagenase 3 (Matrix Metalloproteinase-13) Expression by Osteoblast-like Cells

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