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[RC] Tendon health/exercise - Ridecamp Guest

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Authors M Tsuzaki, D Bynum, L Almekinders, J Faber, AJ Banes
Title   Mechanical loading stimulates ecto-ATPase activity in human tendon cells
Full source     Journal of Cellular Biochemistry, 2005, Vol 96, Iss 1, pp 
117-125

Response to external stimuli such as mechanical signals is critical for normal 
function of cells, especially when subjected to repetitive motion. Tenocytes 
receive mechanical stimuli from the load-bearing matrix as tension, 
compression, and shear stress during tendon gliding. Overloading a tendon by 
high strain, shear, or repetitive motion can cause matrix damage. Injury may 
induce cytokine expression, matrix metalloproteinase (MMP) expression and 
activation resulting in loss of biomechanical properties. These changes may 
result in tendinosis or tendinopathy. Alternatively, an immediate effector 
molecule may exist that acts in a signal-dampening pathway. Adenosine 
5'-triphosphate (ATP) is a candidate signal blocker of mechanical stimuli. ATP 
suppresses load-inducible inflammatory genes in human tendon cells in vitro. 
ATP and other extracellular nucleotide signaling are regulated efficiently by 
two distinct mechanisms: purinoceptors via specific receptor-ligand binding and 
ecto-nucleotidases via the hydrolysis of specific nucleotide substrates. ATP is 
released from tendon cells by mechanical loading or by uridine 5'-triphosphate 
(UTP) stimulation. We hypothesized that mechanical loading might stimulate 
ecto-ATPase activity. Human tendon cells of surface epitenon (TSC) and internal 
compartment (TIF) were cyclically stretched (1 Hz, 0.035 strain, 2 h) with or 
without ATP. Aliquots of the supernatant fluids were collected at various time 
points, and ATP concentration (ATP) was determined by a luciferin-luciferase 
bioluminescence assay. Total RNA was isolated from TSC and TIF (three patients) 
and mRNA expression for ecto-nucleotidase was analyzed by RT-PCR. Human tendon 
cells secreted ATP in vitro (0.5-1 nM). Exogenous ATP was hydrolyzed within 
minutes. Mechanical load stimulated ATPase activity. ATP was hydrolyzed in 
mechanically loaded cultures at a significantly greater rate compared to no 
load controls. Tenocytes (TSC and TIF) expressed ecto-nucleotidase mRNA (ENTPD3 
and ENPP1, ENPP2). These data suggest that motion may release ATP from tendon 
cells in vivo, where ecto-ATPase may also be activated to hydrolyze ATP 
quickly. Ecto-ATPase may act as a co-modulator in ATP load-signal modulation by 
regulating the half-life of extracellular purine nucleotides. The extracellular 
ATP/ATPase system may be important for tendon homeostasis by protecting tendon 
cells from responding to excessive load signals and activating injurious 
pathways.


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