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Alpha-2 adrenergic stimulation triggers Achilles tenocyte hypercellularity : comparison between two model systems

Backman, Ludvig J (författare)
Umeå universitet,Anatomi
Andersson, Gustav (författare)
Umeå universitet,Anatomi
Fong, Gloria (författare)
Umeå universitet,Anatomi,Department of Physical Therapy, University of British Columbia and Centre for Hip Health and Mobility, Vancouver Coastal Health and Research Institute, Vancouver, British Columbia, Canada
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Alfredson, Håkan (författare)
Umeå universitet,Idrottsmedicin
Scott, A (författare)
University of British Columbia, Vancouver, Vancouver Coastal Health and Research Institute
Danielson, Patrik, 1980- (författare)
Umeå universitet,Anatomi
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 (creator_code:org_t)
2012-01-31
2013
Engelska.
Ingår i: Scandinavian Journal of Medicine and Science in Sports. - : John Wiley & Sons. - 0905-7188 .- 1600-0838. ; 23:6, s. 687-696
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • The histopathology of tendons with painful tendinopathy is often tendinosis, a fibrosis-like condition of unclear pathogenesis characterized by tissue changes including hypercellularity. The primary tendon cells (tenocytes) have been shown to express adrenoreceptors (mainly alpha-2A) as well as markers of catecholamine production, particularly in tendinosis. It is known that adrenergic stimulation can induce proliferation in other cells. The present study investigated the effects of an exogenously administered alpha-2 adrenergic agonist in an established in vivo Achilles tendinosis model (rabbit) and also in an in vitro human tendon cell culture model. The catecholamine producing enzyme tyrosine hydroxylase and the alpha-2A-adrenoreceptor (α(2A) AR) were expressed by tenocytes, and alpha-2 adrenergic stimulation had a proliferative effect on these cells, in both models. The proliferation was inhibited by administration of an α(2A) AR antagonist, and the in vitro model further showed that the proliferative alpha-2A effect was mediated via a mitogenic cell signaling pathway involving phosphorylation of extracellular-signal-regulated kinases 1 and 2. The results indicate that catecholamines produced by tenocytes in tendinosis might contribute to the proliferative nature of the pathology through stimulation of the α(2A) AR, pointing to a novel target for future therapies. The study furthermore shows that animal models are not necessarily required for all aspects of this research.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Hälsovetenskap -- Idrottsvetenskap (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Health Sciences -- Sport and Fitness Sciences (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

Nyckelord

tendinopathy
exercise
cytokines
neurotrophins
alpha(2A) adrenoreceptor
Tendinosis
Achilles tendon

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