Article

Fluid-induced shear stress stimulates Ca2+ signaling in human tendon epitenon cells

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Abstract

Tendon cells reside in an environment rich in mechanical stimuli and respond to these stimuli with a variety of activities. Whole tendon, ex vivo, responds to cyclic stretch by increasing DNA and collagen synthesis (Banes et al., 1999). Cultured epitenon and internal cells from tendon respond synergistically to cyclic tensile strain and a growth factor (Banes et al., 1995). Tendon cells stimulated by plasma membrane indentation with a micropipet propagate intercellular calcium waves to neighboring cells via gap junctions (Kenamond et al., 1997). Tendon cells subjected to equibiaxial cyclic stretching signal with a transient rise in intracellular calcium (Kenamond et al., 1998). Recently, it has been shown that connective tissue cells are responsive to fluid-induced shear stress similar to cells of the vascular system. Moreover, Brown and coworkers have shown that apparati used to apply substrate tension to cultured cells have limitations that include a potentially confounding component of fluid-induced shear stress (Brown et al., 1998). Hence, there is a concern that a given cell response to substrate stretching may actually involve a response to shear stress or some combination of the two stimuli. We have designed a parallel plate, laminar flow apparatus that provides regulated fluid-induced shear stress and subjected tendon cells to shear stresses of 0, 5, 10, 15 and 20 dynes/cm2. This will enable us to make a direct comparison between fluid-induced shear stress and substrate deformation on tendon cell signaling and downstream gene responses.

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... Human tendon, ligament (both ACL and MCL), and intervertebral disc annulus cells signal by an increase in intracellular calcium in response to a mechanical stimulus [13][14][15][16] . Chondrocytes in monolayer also signal in response to mechanical stimuli and to ATP-stimulation by increasing their [Ca 2+ ] ic 17,18 . ...
Article
Objective In vivo, chondrocytes are surrounded by an extracellular matrix, preventing direct cell-to-cell contact. Consequently, intercellular communication through gap junctions is unlikely. However, signaling at a distance is possible through extracellular messengers such as nitric oxide (NO) and nucleotides and nucleosides, adenosine triphosphate (ATP), uridine triphosphate (UTP), or adenosine diphosphate (ADP). We hypothesized that chondrons, chondrocytes surrounded by their native pericellular matrix, increase their intracellular calcium concentration ([Ca2+]ic) in response to ATP and other signaling molecules and that the source of Ca2+is from intracellular stores. The objectives of this study were to determine if chondrons in a 3-D gel respond to ATP by increasing [Ca2+]icthrough a purinoceptor mechanism and to test whether chondrons in whole tissue samples would respond to ATP in a similar fashion.
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