Modulation of cell functions of human tendon fibroblasts by different repetitive cyclic mechanical stress patterns
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Cited by (52)
A cell state splitter and differentiation wave working-model for embryonic stem cell development and somatic cell epigenetic reprogramming
2012, BioSystemsCitation Excerpt :Of course, since each mechanical event of contraction or expansion of the apical surface of the cell is actually a mechanochemical event, we may find ways to intervene and accomplish execution of the differentiation code biochemically. The role of mechanics in stem cells is a burgeoning field, suggesting that its role may indeed be more than incidental (Bakker et al., 2004; Barkhausen et al., 2003; Kobayashi et al., 2004; Park et al., 2004; Pearson, 2003; Schild and Trueb, 2004; Simmons et al., 2003; Wang et al., 2001; Yamamoto et al., 2002; Yoshino et al., 2003)…” (Gordon, 2006). Supporting this model are the observable contraction and expansion waves on the surface of urodele amphibian embryos (Gordon and Björklund, 1996) that have trajectories corresponding to the formation of classically defined tissues (Gordon et al., 1994).
Multiscale strain analysis of tissue equivalents using a custom-designed biaxial testing device
2012, Biophysical JournalCitation Excerpt :The physical aspect of cell-extracellular matrix (ECM) interactions is known to be a powerful modulator of cell fate both in vitro and in vivo (1,2). In particular, in vitro systems consisting of engineered tissue equivalents (cells plus substrate/matrix) have been specially designed and used to demonstrate that fundamental cell behaviors, including proliferation, differentiation, and migration, as well as matrix remodeling and metabolism are modulated by mechanical-based microenvironmental cues such as the density and spatial distribution of cell adhesion ligands and substrate/matrix stiffness (3–8). It is also well established that cells respond to externally applied deformation or strain as induced by mechanical loads including hydrostatic pressure, fluid shear, compression, and extension (9).
In vitro modeling of repetitive motion injury and myofascial release
2010, Journal of Bodywork and Movement TherapiesCitation Excerpt :Cyclic strain has been found to cause increases in apoptosis in mesenchymal stem cells (Kearney et al., 2008), vascular endothelial cells (Kou et al., 2009), and periodontal ligament cells (Zhong et al., 2008). Fibroblasts apoptosis in response to cyclic strain has been mixed with increases seen from minutes (Skutek et al., 2003) to days (Barkhausen et al., 2003), decreases (Danciu et al., 2004) and no change (Persoon-Rothert et al., 2002; Nishimura et al., 2007). Thus, the rate of apoptosis appears to be highly dependant on sampling time.
Molecular Events of Cellular Apoptosis and Proliferation in the Early Tendon Healing Period
2010, Journal of Hand SurgeryEngineering human neo-tendon tissue in vitro with human dermal fibroblasts under static mechanical strain
2009, BiomaterialsCitation Excerpt :Moreover, after 26 weeks of implantation under mechanical loading, dermal fibroblast engineered tendon produced predominantly type I collagen (character of tendon), but not both types I and III collagens (character of skin), indicating a possible phenotype switch from dermal fibroblasts to tenocytes with long term mechanical loading and tissue remodeling [5]. Tension is part of in vivo niche of tendon tissue and plays an important role in tenocyte function as mechanical strain has been shown to promote matrix production [17–20]. By contrast, phenotype drift and functional loss have been observed in the in vitro expanded tenocytes, including decreased expression of decorin and increased collagen III/I ratio [21,22].
Retendo (mucopolygen complex) effects on achille tendon healing
2020, Journal of OrthopaedicsCitation Excerpt :In late phases of apoptosis, inflammatory cytokines released from these cells (such as insulin-like growth factor β) prevent inflammatory reaction.10,11 It is known that apoptosis occurs in tendon fibroblast cultures, animal models in which recurrent stretching were applied and also in chronic tendinopathy biopsy materials.12,13 In studies made with rat patellar tendon allografts, it was shown that allograft was the weakest in the fourth week (nearly 20% of its normal strength) (54).