2003
DOI: 10.1016/s0273-1177(03)90395-4
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Microgravity and bone cell mechanosensitivity

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Cited by 73 publications
(47 citation statements)
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“…Alternatively, changes in the cellular physical environment could elicit pathological consequences, even when the cellular mechanotransduction processes function properly. Examples for this scenario include disturbed fluid shear stress at bifurcations that trigger vascular remodelling that can result in the development of atherosclerosis19, or the loss of bone mass in a microgravity environment20. In these cases, it is the abnormal mechanical stress at the cellular level that–through (normal) mechanotransduction signalling–modulates cellular processes that can result in break-down of normal tissue function.…”
Section: Mechanotransduction and Diseasementioning
confidence: 99%
“…Alternatively, changes in the cellular physical environment could elicit pathological consequences, even when the cellular mechanotransduction processes function properly. Examples for this scenario include disturbed fluid shear stress at bifurcations that trigger vascular remodelling that can result in the development of atherosclerosis19, or the loss of bone mass in a microgravity environment20. In these cases, it is the abnormal mechanical stress at the cellular level that–through (normal) mechanotransduction signalling–modulates cellular processes that can result in break-down of normal tissue function.…”
Section: Mechanotransduction and Diseasementioning
confidence: 99%
“…Local factors including cytokines, prostaglandins, leukotrienes, nitric oxide and growth factors, which are produced locally by bone cells, influence the osteoblast-osteoclast interplay (Raisz and Prestwood, 2000). Bone loss caused by exposure to microgravity has been observed in astronauts (Klein-Nulend et al, 2003). A space flight study of Nabavi et al (2011) revealed that osteoblasts exposed to microgravity had smaller and fewer focal adhesions, thinner cortical actin and stress fibres as well as extended cell shapes.…”
Section: Introductionmentioning
confidence: 99%
“…Alterations in tissue loading can cause resultant changes in cellular tensional homeostasis, or the balance between the external forces exerted on cells by their surrounding matrix and internal contractile forces generated by the cells themselves [6,9,12]. Loss of this tensional homeostasis due to changes in the cellular physical environment is known to promote pathologies such as atherosclerosis [13] and bone loss [14]. Previous studies from our lab have shown that, in tendon cells in situ, loss of tensional homeostasis in response to an absence of normal loading produces biological changes which are commensurate with those seen in tendinopathy: increased collagenase production, apoptosis, alterations in the morphology of the tenocytes, and a loss of collagen orientation and packing [8,10,15,16].…”
Section: Introductionmentioning
confidence: 99%