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This study examines the differences between cells in three tendons of horse legs, finding that the number of cells, their growth rate, and their ability to produce certain proteins varies between tendons. These traits may contribute to the differing rates of injury and healing among these tendons.
Research was conducted to ascertain the differences in features of tendinocytes (cells within tendons) from three specific tendons in a horse’s forelimb: the Superficial Digital Flexor Tendon (SDFT), Deep Digital Flexor Tendon (DDFT), and the Common Digital Extensor Tendon (CDET). The properties examined included:
Significant variations were discovered in the number of cells in vivo (within the living organism). The SDFT housed the largest cell number, while the CDET held the least numerable cells. Similarly, in vitro (lab-based) studies showed that the proliferation ratios, collagen synthesis ability, and MMPs synthesis ability were most significant in the SDFT and least in the CDET.
Flexor tendons in forelimbs (SDFT and DDFT) which contract to bend a limb, are more prone to injury and are found to regenerate quicker than extensor tendons, possibly because of their active synthesis of ECM and MMPs.
In contrast, CDET has a remarkably low turnover potential; these tendons exhibit fewer cells, low cellular proliferation, and a diminished ability for collagen and MMPs synthesis.
Adding TNFalpha, a cell signaling protein (cytokine) involved in systemic inflammation, to the cultured tendinocytes increased the synthesis of proMMP-9 (except in the case of CDET) and collagen, while decreasing proMMP-13 synthesis. TNFalpha did not affect proMMP-2 synthesis. This result suggests a potential impact of TNFalpha on injury and healing processes in these tendons.
The isolated tendinocytes furnished crucial information about the characteristics and properties of these tendons. This knowledge contributes to understanding ECM turnover system – the dynamic remodeling of the network of macromolecules providing structural and biochemical support to cells – and how tendinocytes respond to complex inflammatory responses in tendinopathy, which involves tendon inflammation and degeneration frequently leading to injury.
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