Modulation of collagen gel compaction by extracellular ATP is MAPK and NF-kappaB pathways dependent.

Understanding the mechanisms that regulate mechanosensitivity in osteoblasts is important for controlling bone homeostasis and the development of new drugs to combat bone loss. It is believed that prestress or force generation (the tensile stress within the cell body) plays an important role in regulating cellular mechanosensitivity. In the present study, a three-dimensional (3D) collagen culture was used to monitor the change in prestress of the osteoblast-like cells.

Distributing a fixed amount of cyclic loading to tendon explants over longer periods induces greater cellular and mechanical responses.

Tendon overuse injuries are a major source of clinical concern. Cyclic loading causes material damage and induces biochemical responses in tendon. The purpose of this study was to examine the biochemical and biomechanical tendon response after applying cyclical loading over varying durations.

Cyclic loading alters biomechanical properties and secretion of PGE2 and NO from tendon explants.

Background: Tendon overuse injuries are a common occurrence; accounting for a large proportion of occupational and athletic injuries. The concept examined in this study is the role of load-induced intrinsic inflammation to the mechanism of these injuries. This study examined the influence of cyclical loading on the mechanical properties, cell viability, and inflammatory mediators of cultured tendon explants.

Norepinephrine-induced calcium signaling and expression of adrenoceptors in avian tendon cells.

Sympathetic efferent nerves are present in tendons, but their function within tendon is unknown. alpha(1)-Adrenoceptors are expressed by a variety of cell types. In the presence of norepinephrine (NE), adrenoceptors activate G(q/11) signaling pathways that subsequently increase intracellular Ca(2+) concentration ([Ca(2+)](ic)).

Vibratory loading decreases extracellular matrix and matrix metalloproteinase gene expression in rabbit annulus cells.

Background Context: Whole body vibration is an important factor contributing to low back and radicular pain. Vibratory loading as a mechanical stimulus is transferred to connective tissues as energy from ground reaction forces, as well as a direct input from the use of motorized tools and vehicles. Extracellular matrix degradation parallels increased age and mechanical stimuli resulting in disc degeneration and eventual spinal deformity.

Annulus cells release ATP in response to vibratory loading in vitro.

Mechanical forces regulate the developmental path and phenotype of a variety of tissues and cultured cells. Vibratory loading as a mechanical stimulus occurs in connective tissues due to energy returned from ground reaction forces, as well as a mechanical input from use of motorized tools and vehicles. Structures in the spine may be particularly at risk when exposed to destructive vibratory stimuli.

Rabbit tendon cells produce MMP-3 in response to fluid flow without significant calcium transients.

Forces applied to tendon during movement cause cellular deformation, as well as fluid movement. The goal of this study was to test the hypothesis that rabbit tendon fibroblasts detect and respond to fluid-induced shear stress. Cells were isolated from the paratenon of the rabbit Achilles tendon and then subjected to fluid flow at 1 dyn/cm(2) for 6h in a specially designed multi-slide flow device.

Stretch and interleukin-1beta induce matrix metalloproteinases in rabbit tendon cells in vitro.

Little is known about the factors that initiate and propagate tendon overuse injuries, but chronic inflammation and matrix destruction have been implicated. The purpose of this study was to evaluate the production of cyclooxygenase II (COX-2) and matrix metalloproteinases (MMPs) by tendon cells exposed to cyclic strain and inflammatory cytokines in vitro. Rabbit Achilles tendon cells were subjected to a stretching protocol with 5% elongation at 0.