Effects of repetitive motion on human fibroblasts

Almekinders, Louis C.; Banes, Albert J.; Ballenger, Cynthia A.

doi:10.1249/00005768-199305000-00012

Cited by 124 publications

(64 citation statements)

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“…This is because fibroblasts exhibit low mitotic activities under normal physiological conditions (Ahmed et al, 1998) and our in vitro system mimics closely in vivo conditions of tendon fibroblasts (cell shape, alignment, and uniaxial stretching). Previous studies also show that cyclic stretching increased DNA synthesis of human flexor tendon fibroblasts (Almekinders et al, 1993) and proliferation of HPTFs (Zeichen et al, 2000). Moreover, cyclic mechanical stretching has also been reported to increase proliferation of other types of cells, including melanocytes (Kippenberger et al, 1999) and osteoblasts (Neidlinger-Wilke et al, 1995).…”

Section: Discussionmentioning

confidence: 78%

Proliferation and collagen production of human patellar tendon fibroblasts in response to cyclic uniaxial stretching in serum-free conditions

Yang

Crawford

Wang

2004

Journal of Biomechanics

259

195

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Section: Discussionmentioning

confidence: 78%

Proliferation and collagen production of human patellar tendon fibroblasts in response to cyclic uniaxial stretching in serum-free conditions

Yang

Crawford

Wang

2004

Journal of Biomechanics

259

195

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“…Moreover, the production of PGE2 increased in tendons during exercise in animals [72,73] and the production of COX-1, -2 and PGE2 also increased in human tendon fibroblasts after repetitive mechanical loading in vitro [74,75]. Repeated intratendinous injection of PGE2 was reported to lead to focal hypercellularity and matrix degeneration in the patellar tendon of rabbits similar to those seen in tendinopathy [75].…”

Section: Biological Factorsmentioning

confidence: 80%

“…Despite the fact that tenocytes were not capable of differentiating into nontenocyte lineages [7], they might also be involved in the development of tendinopathy through direct interaction with TDSCs or production of inflammatory mediators [74,97,98] and tissue degradative enzymes (matrix metalloproteinases, MMPs) [99], which might in terms affect TDSC functions. The interaction between TDSCs and tenocytes remains undefined.…”

Section: Other Potential Niche Factorsmentioning

confidence: 99%

Tendon-Derived Stem Cells (TDSCs): From Basic Science to Potential Roles in Tendon Pathology and Tissue Engineering Applications

Lui

Chan

2011

Stem Cell Rev and Rep

142

119

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Traditionally, tendons are considered to only contain tenocytes that are responsible for the maintenance, repair and remodeling of tendons. Stem cells, which are termed tendon-derived stem cells (TDSCs), have recently been identified in tendons. This review aims to summarize the current information about the in vitro characteristics of TDSCs, including issues related to TDSC isolation and culture, their cell morphology, immunophenotypes, proliferation and differentiation characteristics and senescence during in vitro passaging. The challenges in studying the functions of these cells are also discussed. The niche where TDSCs resided essentially provides signals that are conducive to the maintenance of definitive stem cell properties of TDSCs. Yet the niche may also induce pathologies by imposing an aberrant function on TDSCs or other targets. The possible niche factors of TDSCs are herein discussed. We presented current evidences supporting the potential pathogenic role of TDSCs in the development of tendinopathy with reference to the recent findings on the altered biological responses of these cells in response to their potential niche factors. The use of resident stem cells may promote engraftment and differentiation of transplanted cells in tendon and tendon-bone junction repair because the tendon milieu is an ideal and familiar environment to the transplanted cells. Evidences are presented to show the potential advantages and results of using TDSCs as a new cell source for tendon and tendon-bone junction repair. Issues pertaining to the use of TDSCs for tissue repair are also discussed.

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“…A fundamental paradox in bone tissue is that tissue-level strains in whole bone due to animal and human locomotion are typically Ͻ0.2% (1,2), yet an extensive range of in vitro experiments in bone (3)(4)(5) and other tissue cultures (6,7) show that dynamic substrate strains must be at least an order of magnitude larger for intracellular biochemical responses to occur. Such large whole-tissue strains in vivo would cause bone fracture.…”

mentioning

confidence: 99%

Mechanotransduction and strain amplification in osteocyte cell processes

Han

Cowin

Schaffler

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

422

319

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A paradox in bone tissue is that tissue-level strains due to animal and human locomotion are too small to initiate intracellular chemical responses directly. A model recently was proposed to resolve this paradox, which predicts that the fluid flow through the pericellular matrix in the lacunar-canalicular porosity due to mechanical loading can induce strains in the actin filament bundles of the cytoskeleton that are more than an order of magnitude larger than tissue level strains. In this study, we greatly refine this model by using the latest ultrastructural data for the cell process cytoskeleton, the tethering elements that attach the process to the canalicular wall and their finite flexural rigidity EI. We construct a much more realistic 3D model for the osteocyte process and then use large-deformation ''elastica'' theory for finite EI to predict the deformed shape of the tethering elements and the hoop strain on the central actin bundle. Our model predicts a cell process that is 3 times stiffer than in a previous study but hoop strain of >0.5% for tissue-level strains of >1,000 microstrain at 1 Hz and >250 microstrain at frequencies >10 Hz. We propose that this strainamplification model provides a more likely hypothesis for the excitation of osteocytes than the previously proposed fluid-shear hypothesis.actin filament bundle ͉ bone mechanotransduction ͉ osteocyte process ͉ strain amplification A fundamental paradox in bone tissue is that tissue-level strains in whole bone due to animal and human locomotion are typically Ͻ0.2% (1, 2), yet an extensive range of in vitro experiments in bone (3-5) and other tissue cultures (6, 7) show that dynamic substrate strains must be at least an order of magnitude larger for intracellular biochemical responses to occur. Such large whole-tissue strains in vivo would cause bone fracture. You et al. (8) recently proposed a new hypothesis and exploratory quantitative cellular-level model that predicts that the fluid flow through the pericellular matrix in the lacunarcanalicular porosity due to small whole-tissue deformations can induce cellular-level strains in the actin filament bundles of the cell processes, which are 1-2 orders of magnitude larger than whole-tissue strains and sufficient to initiate intracellular signaling. This model was intended to demonstrate the quantitative feasibility of the basic hypothesis and not realistically simulate the strain-amplification mechanism, because there was only fragmentary and sometimes contradictory evidence with regard to the key structural components of osteocytes that would be necessary for the model to work in vivo. In addition, there was no information on the most important mechanical properties in the system, i.e., the flexural rigidity EI of the transverse filaments in the pericellular space and the sieving characteristics of the pericellular matrix. You et al. (8) treat these filaments as inextensible strings with no flexural rigidity.The four basic structural components in the model are as follows: (i) transverse filamen...

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Effects of repetitive motion on human fibroblasts

Cited by 124 publications

References 0 publications

Proliferation and collagen production of human patellar tendon fibroblasts in response to cyclic uniaxial stretching in serum-free conditions

Proliferation and collagen production of human patellar tendon fibroblasts in response to cyclic uniaxial stretching in serum-free conditions

Tendon-Derived Stem Cells (TDSCs): From Basic Science to Potential Roles in Tendon Pathology and Tissue Engineering Applications

Mechanotransduction and strain amplification in osteocyte cell processes

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